Biomedical Therapy - International Academy of Homotoxicology

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Biomedical
Therapy
J o urnal o f
Volume 5, Number 1 ) 2011
Integrating Homeopathy
and Conventional Medicine
Female
Disorders
• Current Trends in Women’s Health
• Which Came First: Insulin Resistance or Inflammation?
Contents
I n Fo c u s
© fixerOO/Fotolia.de
Current Trends in Women’s Health . . . . . . . . . . . . . . . . . . . . . . 4
W h a t E l s e I s N e w ? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12
From the Practice
Uterine Fibroids: A Clinical Case Report . . . . . . . . . . . . . . . . . .14
Re f r e s h Yo u r H o m o t ox i c o l o g y
© iStockphoto.com/© DNY59
© iStockphoto.com/Rosemarie©Gearhart
iStockphoto.com/© Anatoliy Samara
Which Came First: Insulin Resistance or Inflammation? . . . .16
Practical Protocols
Genital Human Papilloma Virus Infection
Bioregulatory Management . . . . . . . . . . . . . . . . . . . . . . . .
20
Specialized Applications
Contributions of Biological Medicine in Infertility . . . . . . . . .22
Meet the Expert
Dr. Mónica Lucia Name Guerra . . . . . . . . . . . . . . . . . . . . . . . . .25
E x p a n d Yo u r Re s e a r c h K n o wl e d g e
Purpose-Orientated Clinical Research . . . . . . . . . . . . . . . . . . .26
Around the Globe
Fifth International Congress on
Complementary Medicine Research . . . . . . . . . . . . . . . . . . . . 29
Re s e a r c h H i g h l i g h t s
Traumeel for the Treatment of
Pain Associated With Breast Cancer . . . . . . . . . . . . . . . . . . . . . 30
Cover © Sebastian Kaulitzki/medicstock.com
)2
Published by/Verlegt durch: International Academy for Homotoxicology GmbH, Bahnackerstraße 16,
76532 Baden-Baden, Germany, www.iah-online.com, e-mail: journal@iah-online.com
Editor in Chief/verantwortlicher Redakteur: Dr. Alta A. Smit
Editor: Dr. David W. Lescheid
Managing Editor: Silvia Bartsch
Print/Druck: Dinner Druck GmbH, Schlehenweg 6, 77963 Schwanau, Germany
© 2011 International Academy for Homotoxicology GmbH, Baden-Baden, Germany
© iStockphoto.com/Milena Lachowicz
)
)
Female Health in the 21st Century
Dr. Alta A. Smit
T
he woman of today lives in a
changed environment, which
plays a decisive role in the development of disease. The sociocultural
environment has changed through
shifting roles of women in society,
who are often late parents and also
support aging parents on top of
their own families and work.1 The
psychological stresses normal for
our modern lives are often amplified
by the dual role of career woman
and housewife.
The physical environment also has a
substantial influence on women’s
health. Environmental toxins have
been implicated as so-called endocrine disruptors and as triggers for
metabolic syndrome, which in itself
is closely associated with female diseases, such as polycystic ovary syndrome and infertility.2,3
Thus, the triad of chronic psychological stress, environmental toxicity, and obesity with the concomitant
systemic inflammation forms the
background for many female disorders. This triad often becomes a circulus vitiosus.,
The eating patterns of modern
women have changed, with stress
eating being the order of the day.4
This is combined with a change in
the activity of the hypothalamic-pituitary-adrenal axis. The resultant
obesity increases systemic inflammation and increases the storage of
fat-soluble toxins, such as the organochlorides, noted endocrine disruptors.5,6
In this issue, Dr. Michael Greer, a
gynecologist, examines the current
trends in women’s health and suggests possible treatment strategies.
Dr. Olga García reports on a case of
uterine fibroids, treated with bioregulatory medicine, while Dr. Gaston Orellana has two contributions,
one on infertility and one on the
treatment of chronic postmastectomy pain, which won him the Recke
weg Incentive Award in 2008.
As mentioned earlier, we see an increasing link between inflammation
and metabolic disturbance. Dr. David Lescheid examines this phenomenon in his cutting-edge article on
the link between insulin resistance
and inflammation.
Dr. Robbert van Haselen continues
the series on research methodologies, and Dr. Konstantin Cesnulevicius reports on a complementary
research congress in Tromsø, Norway.
Journal of Biomedical Therapy 2011 ) Vol. 5, No. 1
Last, we introduce an expert wellknown to many as an excellent
lecturer with a beautiful voice:
Dr. Mónica Name.
Dr. Alta A. Smit
References
1. Ron P. Daughters as caregivers of aging
parents: the shattering myth. J Gerontol Soc
Work. 2009;52(2):135-153.
2. Desvergne B, Feige JN, Casals-Casas C.
PPAR-mediated activity of phthalates: a link
to the obesity epidemic? Mol Cell Endocrinol.
2009;304(1-2):43-48.
3. Mendola P, Messer LC, Rappazzo K. Science
linking environmental contaminant exposures with fertility and reproductive health
impacts in the adult female. Fertil Steril.
2008;89(suppl 2):e81-e94.
4. Torres SJ, Nowson CA. Relationship between
stress, eating behavior, and obesity. Nutrition.
2007;23(11-12):887-894.
5. Elobeid MA, Padilla MA, Brock DW, Ruden
DM, Allison DB. Endocrine disruptors and
obesity: an examination of selected persistent
organic pollutants in the NHANES 19992002 data. Int J Environ Res Public Health.
2010;7(7):2988-3005.
6. Müllerová D, Kopecký J. White adipose tissue: storage and effector site for environmental pollutants. Physiol Res. 2007;56(4):375381.
)3
) I n Fo c u s
Current Trends
in Women’s Health
By Michael E. Greer, MD
Obstetrician/Gynecologist
Introduction
)4
After World War II, modern life
brought special challenges for women’s health and family planning. Today, there is a growing trend for
women to delay having their first
baby until later in life to establish a
career before embarking on parenthood; in addition, middle-aged
women who remarry may want to
add to their existing family with
their new partner. Many epidemiological data investigating maternal
age and fetal loss have confirmed
that older age strongly increases a
woman’s chances of stillbirth, miscarriage, and ectopic pregnancy.1
Older women carry risks of conceiving a trisomic oocyte and of
having a less efficient uterus.2 Conversely, women who chose to have
children early in life are returning to
work and working longer into the
perimenopausal and menopausal
years (the so-called baby boomers
turned zoomers). It is generally accepted that susceptibility to stress
and stress-related illness can be affected by hormonal changes and
that common menopausal symptoms (eg, tiredness and night sweats)
can make women temporarily more
susceptible to fatigue and stress at
work. In addition to these trends in
culture, the options for controlling
fertility have grown during the past
50 years, affecting the age at which
women bear children.2 Specifically,
“pills” or oral contraceptives (OCs)
contain hormones that suppress
ovulation, thicken the cervical mucous to block sperm passage, and/or
cause abortion by making the uterine lining hostile to implantation.
Oral contraceptives have been used
in the management of premenstrual
symptoms3 and, although not sufficiently substantiated, endometriosis.4 Combined OCs have a significant protective effect on the risk of
ovarian and endometrial cancer,
which increases with duration of
use, and can be used as chemoprevention in young women who are
breast cancer gene (BRCA) mutation
carriers.5 Indeed, none of the large
prospective cohort studies with prolonged follow-up has indicated an
increased overall risk of cancer incidence or mortality among women
that have ever used OCs.5 However,
OC use has been associated with an
increased risk of venous thromboembolism.6 There is also a slightly
increased breast cancer risk among
current OC users that disappears 5
to 10 years after discontinuation, an
increased cervical cancer risk with
long-term OC use, and an increased
risk of benign liver tumors and liver
cancer.5
However, the options surrounding
fertility are not always a matter of
choice. Among the many chemicals
and toxins released into the environment during the past decades, the
endocrine disruptors can interfere
with the endocrine system through
their binding to intracellular receptor proteins for steroid hormones.7
In particular, endocrine disruptors
have a strong impact on the normal
functioning of the reproductive system.7,8 They ultimately interfere
with the effects of endogenous steroid hormones, evoking hormonal
effects in animals, humans, and cell
cultures.8 For example, bisphenol A,
used in the manufacture of plastics,
has been associated with many different malformations of the female
reproductive tract, including cystic
ovaries, in animal models.7 Moreover, the detrimental effects on reproductive physiological features in
animals by other medicines, such as
nonsteroidal
anti-inflammatory
drugs, after long-term inhibition of
prostaglandins in humans remain
unknown.9 However, the most dramatic effects of endocrine disruptors
may be the many reproductive organ dysfunctions observed in women exposed in utero to diethylstilbestrol.8
Disorders of the female reproductive system (Figure 1) have a wide
range of etiologies, including infections and hormonal problems. Primary symptoms can vary from va
ginal discomfort and discharge to
chronic debilitating pain. Although
the pathophysiological characteristics of some conditions are wellknown, others are more enigmatic,
with multiorgan involvement and
) I n Fo c u s
Uterus
© fixerOO/Fotolia.de
Fallopian tube
Ovary
Cervix
Endometrial
(uterine) lining
Vagina
Myometrium
Figure 1. Female Reproductive System
multiple potential targets for treatment, and require a comprehensive
approach to patient management.
This article reviews current thinking
on some of the more challenging
conditions affecting female health.
Inflammatory Disorders
Vaginitis
Vaginitis is one of the most common
reasons for women to present to a
family physician.10 In the United
States each year, an estimated 10
million health care office visits to
gynecologists are because of vulvovaginitis.11 Vulvovaginitis is a term
encompassing a variety of inflammatory lower genital tract disorders.11 In addition to infection, other causes of vaginal itching, burning,
irritation, or discharge include allergy to latex condoms, contact dermatitis, and atrophic vaginitis.10
Although the causes of vulvovaginitis are many and varied, women fre-
quently assume they are the result of
a yeast infection or an allergy to a
new product. Consequently, the use
of over-the-counter medications is
very high for this condition. This
can lead to considerable delay between the onset of symptoms and
consultation with a clinician and establishment of a definitive diagnosis.12
Infectious vaginitis can be caused by
several organisms. The most common of these organisms are Gardner
ella vaginalis and Mycoplasma homi
nis, causing bacterial vaginosis
(22%-50%); Candida albicans, causing vulvovaginal candidiasis (17%39%); and Trichomonas vaginalis
causing vaginitis and/or urethritis
(4%-35%). However, coinfections
can exist, and the exact cause of
vaginal symptoms may remain undiagnosed in many women.10
Approximately 75% of women will
have an episode of vulvovaginal
candidiasis within their lifetime;
40% to 45% will have 2 or more
episodes.10 However, many women
with symptoms of recurrent vaginitis do not have candidiasis; consequently, self-treatment with overthe-counter antifungal agents is
ineffective.12 Trichomoniasis is estimated to be responsible for 25% of
vaginitis cases in the United States
and is the most common nonviral
sexually transmitted infection.12
Patients with infectious vaginitis
commonly present with vaginal or
perineal vulvar irritation and abnormal vaginal discharge.10 However,
women with bacterial vaginosis and
trichomonas can be asymptomatic.10
Etiology cannot be confirmed without examination of the discharge
specimen. The gold standard for the
diagnosis of candidiasis is visualization of pseudohyphae (mycelia)
and/or budding yeast on a 10% potassium hydroxide wet preparation;
for bacterial vaginosis, vaginal Gram
stain (Nugent or Spiegel criteria);
)5
http://en.wikipedia.org/wiki/File:Perforierte_
Endometriosezyste.jpg
) I n Fo c u s
Figure 2. Endoscopic Image
of a Ruptured Endometrial Cyst
(“Chocolate Cyst”)
)6
and for T vaginalis, culture (Diamond media or InPouch TV).13 The
treatment of infectious vaginitis depends on the causative organism:
antifungals are used to treat candidiasis; antibiotics, such as metronidazole and clindamycin, are effective against anaerobic bacteria and
are used to treat bacterial vaginosis;
and either metronidazole or tinidazole are usually used to treat T vagi
nalis, a protozoan.10 In conventional
treatment for candidiasis, topical
azoles are the mainstay of treatment,
achieving complete relief of symptoms in 80% to 90% of patients.
However, oral agents are more acceptable and convenient for many
women, although they are associated with adverse effects, such as
headache and gastrointestinal upset,
and are more costly. A single 150mg fluconazole dose will achieve
clearance in approximately two
thirds of patients, whereas a second
dose, given on day 3, will yield an
80% clearance rate. In women with
recurrent infections, longer courses
may be needed to suppress Candida.
Treatment failure may indicate infection with Candida glabrata, which
does not respond well to azoles, in
which case intravaginal boric acid
capsules may be effective.10
Bacterial vaginosis is usually treated
with metronidazole or macrolide
antibiotics, such as clindamycin.12
Although treatment of bacterial
vaginosis reduces symptoms, recur-
rences are common: 23% of women
will have a recurrence at 1 month,
and 58% will experience a recurrence within 1 year.10
Trichomonas is usually treated with
oral nitroimidazoles, such as metronidazole.12 In trichomonas, abstinence from alcohol is recommended
for 24 hours after starting metronidazole treatment and for 72 hours
after taking tinidazole because of
the potential for a disulfiram-like reaction, which may include flushing,
nausea, vomiting, thirst, palpitations, chest pain, vertigo, and hypotension.10
Because trichomonas is a sexually
transmitted infection, and carriers
may be asymptomatic, sexual partners should also be treated to prevent reinfection. Indeed, recurrences
of trichomonas are commonly reinfections or may be a consequence of
nonadherence to medical treatment.10 However, there are cases of
resistance to metronidazole.10
Pelvic Inflammatory Disease
Pelvic inflammatory disease (PID) is
defined as an ascending infection
that spreads from the vagina or cervix to the fallopian tubes, endometrium, ovaries, and peritoneum. It
can lead to any combination of endometritis, salpingitis, tubo-ovarian
abscess, and pelvic peritonitis.14 Pelvic inflammatory disease has the potential for fallopian tube scarring,
chronic pelvic pain, ectopic preg-
nancies, and infertility.10,15 Indeed,
approximately 25% of women who
experience a single episode of PID
experience tubal infertility, chronic
pelvic pain, or an ectopic pregnancy; after a third episode of PID, half
of the women will experience infertility.14
In the developed world, 8% to 15%
of women may be diagnosed as having PID in their lifetime, whereas
much higher rates (up to 32%) are
reported in the developing world.16
Chlamydia trachomatis and Neisseria
gonorrhoeae are the organisms most
commonly implicated in PID.14-16
Swabs of the cervix identify gonorrhea in 30% to 80% of patients and
chlamydia in 20% to 40% of patients.14 There are concerns that recent increases in the incidence of
chlamydia and gonorrhea may be
associated with an increase in the
incidence of PID.15 Pelvic inflammatory disease may develop in up to
40% of women with untreated chlamydia infection and in most women
with untreated gonorrhea.10
Gonorrhea and chlamydia may initiate a polymicrobial infection, including Gram-positive and Gramnegative bacteria and anaerobes.
Therapy requires multiple antibiotic
regimens to ensure that all organisms are treated.10,15,16 Treatment
may be oral or intravenous, depending on the status of the patient and
the patient’s ability and/or willingness to take oral medication.10
) I n Fo c u s
Adequate antibiotic coverage for anaerobic organisms is difficult to
achieve, with metronidazole appearing to have limited efficacy, possibly
because poor tolerability limits
compliance.16 Microbial resistance
to other antibiotics also is a problem.15-17
As a consequence of the prevalence
of antibiotic resistance, modulation
of the innate immune system to protect against infection has been discussed as an attractive alternative to
antibiotic therapies in the medical
literature.18 Study of the innate immune response has indicated that
there is variation in host immunity,
possibly because of genetic differences. Thus, a suboptimal innate immune response may result in a permissive environment for pathogen
colonization, whereas an excessive
response will result in disproportionate levels of inflammation and
tissue damage. An investigation of
modulation of the innate immune
response in the reproductive tract
could provide significant advances
in the management of PID and its
sequelae.18
Endometriosis
Endometriosis can have a profound
impact on a woman’s life, potentially affecting her education, career,
and ability to have children.19 The
cost of endometriosis to both the individual and society, including delayed diagnosis and ineffective treatments, is considerable and poorly
quantified.19 The results of a health
survey in the United States indicated
that half of women reporting endometriosis required at least a day of
bed rest within the past year, as a
consequence of the condition, with
the average number of days of bed
rest being 17.8.20 More than 8% of
women reported that endometriosis
limited their activity, and nearly 5%
reported that it limited them in their
work; only cancer and prolapse provided greater levels of limitation in
this survey.20 Confirming these findings, the first Global Study of Women’s Health reporting the societal
impact of endometriosis found a
significant loss of work productivity
among 1459 women (aged 18-45
years) who have the condition. Loss
of work productivity (not caused by
absence from work) was approximately 10 hours per week vs 7
hours per week for those with other
disorders. Non–work-related activities, such as housework, exercise,
and child care, were also significantly impaired.21
Endometriosis remains an enigmatic
disorder: the etiology, natural history, and mechanisms by which it
causes pain are not completely understood.22,23 Endometriosis is a
condition in which tissue with the
characteristics of endometrial tissue
is located outside the endometrial
cavity.19,22 The most commonly
acepted theory regarding the pathophysiological features of endometriosis is that desquamated
en
do
metrial cells are transported
into the peritoneal cavity after retrograde menstruation, with viable
cells subsequently implanting and
growing.19,24-27
For some patients, endometriosis is
not significant; for others, it is aggressive and invasive, causing incapacitating pain.22 The pain associated with endometriosis commonly
manifests as dysmenorrhea, dyspareunia, and chronic pelvic pain
(noncyclic nonmenstrual pelvic
pain).22
The true prevalence and incidence
of endometriosis are difficult to determine because diagnosis requires
surgical biopsy with histological
confirmation.22 The disorder is more
common in women of reproductive
age,24 with the prevalence estimated
to be between 6% and 15%.19,26,27
The annual incidence of surgically
diagnosed disease is 1.6 per 1000
women aged 15 to 49 years.26 It is
estimated that 5% to 21% of women
with pelvic pain experience endometriosis,25 increasing to approximately 75% of women with chronic
pelvic pain.26 Endometriosis is the
third leading cause of gynecologic
hospitalization in the United
States.26 Approximately half of
women with endometriosis are infertile,25 and endometriosis represents the leading cause of infertility.26
Incomplete knowledge regarding
the pathogenesis and pathophysiological features of endometriosis is a
major obstacle to effective treatment.19 There are several factors that
may be implicated in the pathogenesis of endometriosis, including hormonal dysfunction, aberrant gene
expression, immunoinflammatory
changes, abnormal growth (Figure
2), remodeling, and angiogenesis. It
is believed that all these dysfunctions play a role in the underlying
multifactorial molecular events leading to the development of endometriosis and its symptoms.25
Oxidative stress has been implicated
in endometriosis and infertility. An
imbalance in the generation of reactive oxygen species and the scavenging capacity of antioxidants in the
reproductive tract provides an environment for the development of
oxidative stress.24 Indeed, studies
have shown that oxidative stress and
antioxidant biomarkers are present
in both serum and peritoneal fluid
of women with endometriosis.24
Women with endometriosis may exhibit altered expression of the enzymes involved in the defense
against oxidative stress in the endometrium.24
Antioxidants, such as vitamin E, can
play an important role in protecting
biological membranes by preventing
)7
© iStockphoto.com/Amanda Rohde
) I n Fo c u s
Figure 3. Ultrasound Showing
Typical Ovarian Cysts in Polycystic
Ovary Syndrome
)8
the activation of pathways implicated in abnormal cell proliferation and
inflammatory response. However,
the role of antioxidants in endometriosis is not clear. Although some
studies have found that they can afford some protection against the development of endometriosis, others
have found no improvement.24
There is evidence that endometriosis
is a pelvic inflammatory process.22,26
Indeed, there is emerging evidence
that women with endometriosis are
more likely to have other inflammatory diseases, such as fibromyalgia
and rheumatoid arthritis, than the
general population.26 Endometriosis
generates significant inflammatory
responses, suggesting that much of
the pain associated with endometriosis is inflammatory.22 A theory is
that the presence of inflammation
activates silent nociceptors and significantly enhances both the sensitivity and severity of visceral pain.22
Visceral cross sensitization is
thought to be a factor in the common co-occurrence of other visceral
pain syndromes, such as dyspareunia, interstitial cystitis, and irritable
bowel syndrome.22 It is believed to
be the result of increased persistent
nociceptive input from inflamed reproductive system organs that sensitize neurons, particularly at the dorsal root ganglion; they also receive
input from unaffected visceral organs (eg, bladder and colon). This
phenomenon may underlie comor-
bidity in many functional visceral
pain syndromes.22
Surgery is the first-line treatment
option for endometriosis. Conservative surgical removal of endometriosis provides pain relief and increases
the chances of pregnancy.19 However, this approach is far from ideal.
Although surgery may alleviate pelvic pain in the short-term, it usually
recurs within 2 years. Furthermore,
the spontaneous pregnancy rate after surgery is generally lower than
50%.19 In addition, there are risks
associated with surgery and repeated use of this modality increases the
risk of complications.19 Thus, medical treatment is generally used to
prevent recurrences.
Despite a paucity of evidence, nonsteroidal anti-inflammatory drugs
are often used to treat symptoms.19
Hormonal treatments, such as OCs,
are frequently used with some success, although symptoms often return and may even worsen on cessation.19 An obvious drawback of
hormonal approaches is that they
disrupt the menstrual cycle and do
not offer an option for women who
want to conceive.27 Although research into new treatment options is
ongoing, surgical and medical treatment of endometriosis is far from
satisfactory.19,26,27 Ideally, treatment
should alleviate the pain and address the subfertility associated with
the disease, while not interfering
with ovulation and menstruation. In
addition, treatment should be well
tolerated and have no significant adverse effects or teratogenicity.27
Bioregulatory Treatment
Vaginitis and PID
The bioregulatory treatment of vaginitis and PID is directed toward the
terrain and especially toward the
epithelial barrier and the restoration
of symbiotic microflora. As previously mentioned, it is often difficult
to contain the conditions with only
antimicrobial treatment and it is difficult to deal with recurrences. Treatment options include Gynäcoheel;
because of the low-dose ingredients,
this agent is thought to have an action on inflammatory conditions of
the female genital tract.28 Furthermore, the addition of Mucosa compositum to support the epithelial
barrier is useful. For bacterial infections, Echinacea compositum is used
in an adjuvant fashion, and MetroAdnex-Injeel is added in the case of
PID. Last, if the situation is recurrent, the patient should undergo a
basic detoxification, as described in
previous issues of this journal.29
Probiotics form an essential part of
the treatment of vaginitis and may
even have a preventative role.30,31 It
is essential to restore the flora after
antimicrobial treatment and to ensure a healthy genital tract environment.
) I n Fo c u s
Endometriosis
Bioregulatory therapy has a significant role to play in the treatment of
endometriosis because the condition
presents like a typical dysregulation
syndrome. The immune and neuroendocrine systems, and local tissue
cycles, are involved, making linear
intervention difficult; therefore, endometriosis lends itself to the multitargeted approach that is used in
homotoxicology.
The basic treatment for endometriosis is the inflammation-regulating
drug Traumeel. Ovarium compositum is added, along with Coenzyme
compositum for metabolic support.
Ovarium compositum also contains
hypophysis suis, which supports the
hypothalamic-pituitary-ovarian-adrenal axis. The immunomodulator,
Tonsilla compositum, is used to support the immune system. In addition, Tonsilla compositum contains
hypothalamus suis and glandula suprarenalis suis that further support
the hypothalamic-pituitary-adrenal
axis; and a primitive tissue, funiculus
umbilicalis suis, that is postulated to
support the connective tissue.28
Traumeel is given daily, whereas the
other medications are prescribed in
cycles of 5 weeks, with 4 weeks’ rest
in between (2 ampoules of each are
given orally or subcutaneously twice
a week). The number of cycles needed depends on the response of the
patient.
Metabolic Disorders:
Polycystic Ovary Syndrome
Polycystic ovary syndrome (PCOS)
is the most frequent endocrinopathy
in women of reproductive age,32 occurring in approximately 5% to 10%
of these women.33,34 The Rotterdam
criteria for the diagnosis of PCOS
require 2 of the following 3 criteria
to be met: irregular or no ovulation,
clinical/paraclinical
hyperandro-
genemia, and polycystic ovaries
(Figure 3). Other causes of hyperandrogenemia also need to be excluded.32 Interestingly, confirmation of
the presence of polycystic ovaries is
not necessary for diagnosis.33
Polycystic ovary syndrome can affect women in many different
ways.33 Common manifestations of
PCOS include hirsutism, infertility,
insulin resistance, and menstrual irregularities.33 Other conditions that
may be associated with PCOS include hypertension, dyslipidemia,
and type 2 diabetes mellitus, which
all increase the risk of cardiovascular events, with associated morbidity
and mortality.34,35 Thus, PCOS is
recognized as having a major impact throughout life on the gynecological and metabolic health of
women.34
Treatment of PCOS is frequently
targeted at specific manifestations.
For example, insulin-sensitizing
agents, such as metformin, may be
used to treat insulin resistance; eflor
nithine may be used to treat hirsutism; and OCs may be used to address menstrual irregularities or,
alternatively, clomiphene may be
used to address infertility.33 Treatment should aim to break the vicious cycle of abdominal obesity
and inflammation that lead to increased testosterone levels and, thus,
promote the abdominal obesity/inflammation cycle.32
The prevalence of insulin resistance
is much higher in women with
PCOS compared with an age- and
weight-matched population of
women.33 Insulin resistance is often
a precursor to the development of
diabetes and is a component of the
metabolic syndrome, conferring an
increased cardiovascular risk.33 Approximately 50% to 70% of women
with PCOS have some degree of insulin resistance.35 However, the precise mechanism of insulin resistance
is not clear. It seems most likely that
this is a result of impaired glucose
metabolism, rather than a difference
in the number and affinity of insulin
receptors, making the mechanism of
insulin resistance in PCOS unique.32
In the ovaries, high insulin levels
stimulate the conversion of progesterone to androstenedione, which is
then converted to testosterone. The
theory that hyperinsulinemia may
stimulate hyperandrogenemia in
PCOS is supported by the efficacy
of insulin-sensitizing agents, such as
metformin.32 However, studies using
glitazones suggest that this relationship may be more complex.32 High
testosterone levels in women with
PCOS promote abdominal obesity
that, in turn, promotes insulin resistance, leading to increased testosterone activity; thus, the vicious circle
ensues.32 Polycystic ovary syndrome
is a multiorgan disease: abdominal
obesity and increased activation of
the inflammatory system, seen in
both normal-weight and obese patients with PCOS, lead to an increased risk of dyslipidemia, diabetes, and cardiovascular disease.32
Hormonal imbalance caused by
PCOS can lead to hyperandrogenism that can manifest as hirsutism
and/or acne.33 Hirsutism occurs in
5% to 25% of women of reproductive age.32 Between 70% and 90% of
women with hirsutism are diagnosed as having PCOS.32 Although
many treatments for hirsutism are
nonpharmacological, antiandrogens,
such as spironolactone and finasteride, are sometimes used. However,
OCs are among the most commonly
used medications for hirsutism and
acne.33
The elevated levels of androgens in
women with PCOS can also cause
menstrual irregularities with associated infertility. Although OCs are
often used to address menstrual irregularities, they obviously cannot
)9
© iStockphoto.com/© hartphotography1
) I n Fo c u s
Figure 4. Central obesity is common
in patients with polycystic ovary
syndrome. Increased visceral fat
is associated with a higher risk
of heart disease, hypertension,
insulin resistance, and diabetes
mellitus type 2.
) 10
help with infertility.33 Clomiphene,
an ovulation-induction agent, may
be used, with the risks of multiple
pregnancies, ovarian hyperstimulation, thromboembolism, and visual
disturbances. Alternatively, insulinsensitizing agents, such as metformin, have shown benefit in the
treatment of infertility associated
with PCOS.33
Obesity is prevalent in women with
PCOS.35 Approximately 60% to
70% of patients with PCOS are
obese. Furthermore, the fat is distributed around the central body;
such visceral obesity is associated
with insulin resistance (Figure 4).35
However, although the obesity
found in PCOS contributes to the
level of insulin resistance observed,
the levels of insulin resistance are
greater than those that can be explained purely by the higher levels
of fat.35 The obesity rate has increased considerably in women with
PCOS during the past decades,
whereas the prevalence of PCOS
has increased only minimally. This
suggests that genetic factors may
play a more important role than environmental factors in the development of PCOS.34
Obesity is associated with lowgrade inflammation and increased
inflammatory cytokine levels. Although obesity-related inflammation is often considered a disorder
of innate immunity, there is significant cross talk between the innate
and adaptive immune systems.
Moreover, disorders of both innate and adaptive immunity have
been implicated in obesity-related
inflammation.35 In addition, the inflammatory process associated with
obesity could underlie comorbidities, such as atherosclerosis, diabetes,
and fatty liver disease.35 Indeed, up
to 50% of women with PCOS fulfill
the criteria of the metabolic syndrome.32 Furthermore, the incidence
of diabetes is increased, with an estimated 5- to 8-fold increase in risk
compared with age- and weightmatched controls.32
Weight loss is an important component of PCOS management. Lifestyle modification and weight loss
improve ovulation rate and fertility
and decrease testosterone levels.
Greater than 5% to 10% weight loss
can improve fertility and menstrual
cycles in women with PCOS, although no specific diet has been
identified as particularly effective.32,34
Bioregulatory Treatment:
PCOS
In patients with obesity and PCOS,
the most important intervention is
weight loss because central obesity
significantly contributes to the
whole syndrome.
Bioregulatory treatment includes
Gynäcoheel and Cutis compositum
for symptomatic relief and Ovarium
compositum, Placenta compositum,
Coenzyme compositum, and Ubichinon compositum for organ and
tissue support. Additional supportive treatment with Hepar compositum, Thyreoidea compositum, and
Solidago compositum is also used to
promote the restoration of autoregulatory pathways.
Conclusion
The management of many female
disorders remains challenging, with
a need to address many different
components. As understanding of
the pathophysiological characteristics of these conditions grows,
hopefully more effective treatments
will follow. In the meantime, recognition of the multiorgan involvement in many of these diseases emphasizes the importance of a
comprehensive approach to patient
management.|
) I n Fo c u s
References
1. Andersen A-MN, Wohlfahrt J, Christens P,
Olsen J, Melbye M. Maternal age and fetal
loss: population based register linkage study.
BMJ. 2000;320(7251):1708-1712.
2. Stein Z, Susser M. The risks of having
children in later life: social advantage may
make up for biological disadvantage. BMJ.
2000;320(7251):1681.
3. Shulman LP. Gynecological management of
premenstrual symptoms. Curr Pain Headache
Rep. 2010;14(5):367-375.
4. Vercellini P, Eskenazi B, Consonni D, et
al. Oral contraceptives and risk of endometriosis: a systematic review and metaanalysis [published online ahead of print
September 10, 2010]. Hum Reprod Update.
doi:10.1093/humupd/dmq042.
5. Cibula D, Gompel A, Mueck AO, et al. Hormonal contraception and risk of cancer.
Hum Reprod Update. 2010;16(6):631-650.
6. Tchaikovski SN, Rosing J. Mechanisms of
estrogen-induced venous thromboembolism.
Thromb Res. 2010;126(1):5-11.
7. Massé J, Watrin T, Laurent A, Deschamps S,
Guerrier D, Pellerin I. The developing female
genital tract: from genetics to epigenetics.
Int J Dev Biol. 2009;53(2-3):411-424.
8. Colborn T, vom Saal FS, Soto AM. Developmental effects of endocrine-disrupting chemicals in wildlife and humans. Environ Health
Perspect. 1993;101(5):378-384.
9. Martini AC, Vincenti LM, Santillán ME, et al.
Chronic administration of nonsteroidal-antiinflammatory drugs (NSAIDS): effects upon
mouse reproductive functions. Rev Fac Cien
Med Univ Nac Cordoba. 2008;65(2):47-59.
10. Biggs WS, Williams RM. Common gynaecologic infections. Prim Care Clin Office Pract.
2009;36(1):33-51.
11.Angotti LB, Lambert LC, Soper DE. Vaginitis: making sense of over-the-counter
treatment options. Infect Dis Obstet Gynecol.
2007;2007:97424.
12.Farage MA, Miller KW, Ledger WJ. Determining the cause of vulvovaginal symptoms.
Obstet Gynecol Surv. 2008;63(7):445-464.
13. Centers for Disease Control and Prevention,
Division of STD Prevention. STD Curriculum for Clinical Educatiors: Vaginitis Module, January 2010. http://www2.cdc.gov/
stdtraining/ready-to-use/Manuals/Vaginitis/vaginitis-notes-2010.doc. Accessed May
2, 2011.
14. Trigg BG, Kerndt PR, Aynalem G. Sexually
transmitted infections and pelvic inflammatory disease in women. Med Clin N Am.
2008;92(5):1083-1113.
15.Sweet RL. Treatment strategies for pelvic
inflammatory disease. Expert Opin Pharma
cother. 2009;10(15):823-837.
16. Haggerty CL, Ness RB. Diagnosis and treatment of pelvic inflammatory disease. Womens
Health (Lond Engl). 2008;4(4):383-397.
17. Judlin P. Current concepts in managing pelvic inflammatory disease. Curr Opin Infect
Dis. 2010;23(1):83-87.
18. Horne AW, Stock SJ, King AE. Innate immunity and disorders of the female reproductive
tract. Reproduction. 2008;135(6):739-749.
19. Fedele L, Somigliana E, Frontino G, Benaglia
L, Vigano P. New drugs in development for
the treatment of endometriosis. Expert Opin
Investig Drugs. 2008;17(8):1187-1202.
20. Kjerulff KH, Erickson BA, Langenberg PW.
Chronic gynaecological conditions reported
by US women: findings from the National
Health Interview Survey, 1984 to 1992.
Am J Public Health. 1996;86:195-199.
21. Global Study of Women’s Health (GSWH).
Endometriosis has a significant effect on
women’s work productivity. European Society of Human Reproduction and Embryology (ESHRE) 28 June 2010. http://www.
alphagalileo.org/ViewItem.aspx?ItemId=7
9739&CultureCode=en. Accessed May 2,
2011.
22. Howard FM. Endometriosis and mechanisms
of pelvic pain. J Minimally Invasive Gynecol.
2009;16(5):540-550.
23. Kyama CM, Mihalyi A, Simsa P, Mwenda JM,
Tomassetti C, Meulerman C, D’Hoghe TM.
Non-steroidal targets in the diagnosis and
treatment of endometriosis. Curr Med Chem.
2008;15(10):1006-1017.
24.Augoulea A, Mastorakos G, Lambrinoudaki
I, Christodoulakos G, Creatsas G. The role
of the oxidative-stress in the endometriosis-related infertility. Gynecol Endocrinol.
2009;25(2):75-81.
25. Bondza PK, Maheux R, Akourn A. Insights
into endometriosis-associated endometrial
dysfunctions: a review. Front Biosci (Elite Ed).
2009;1:415-428.
26.Bukulmez O. Endometriosis and the role
of reproductive medicine. Minerva Ginecol.
2009;61(4):299-318.
27.Nothnick WB. Endometriosis: in search
of optimal treatment. Minerva Ginecol.
2010;62(1):17-31.
28. Biotherapeutic Index: Ordinatio Antihomo
toxica et Materia Medica. 7th Rev ed. BadenBaden, Germany: Biologische Heilmittel
Heel GmbH; 2006.
29. Detoxification and drainage. J Biomed Ther.
2007;1(2):3-21.
30. Reid G, Dols J, Miller W. Targeting the vaginal microbiota with probiotics as a means to
counteract infections. Curr Opin Clin Nutr
Metab Care. 2009;12(6):583-587.
31. Zuccotti GV, Meneghin F, Raimondi C, et al.
Probiotics in clinical practice: an overview.
J Int Med Res. 2008;36(suppl 1):1A-53A.
32. Glintborg D, Andersen M. An update on the
pathogenesis, inflammation, and metabolism
in hirsutism and polycystic ovary syndrome.
Gynecol Endocrinol. 2010;26(4):281-296.
33.Radosh L. Drug treatments for polycystic ovary syndrome. Am Fam Physician.
2009;79(8):671-676.
34.Hirschberg AL. Polycystic ovary syndrome,
obesity and reproductive implications.
Womens Health (Lond Engl). 2009;5(5):529540.
35.Sathyapalan T, Atkin SL. Mediators of inflammation in polycystic ovary syndrome
in relation to adiposity. Mediators Inflamm.
2010;2010:758656.
) 11
) What Else Is New?
Moderate physical activity, in particular
© Siggi/Fotolia.de
walking, may prevent stroke in women.
) 12
Walking Reduces Stroke Risk
in Women
Melatonin Helps
Prevent Cancer in Women
Antihomotoxic Therapy
for Autoimmune Thyroiditis
Moderate walking makes a difference in women’s health. A recent
study indicates that walking is associated with lower risks of different
types of stroke, including total, ischemic, and hemorrhagic strokes.
Physical activity has been shown to
modify risk factors for stroke, such
as obesity and hypertension, by decreasing blood pressure and atherosclerosis and improving lipid profile
and insulin sensitivity. The study
included 39,315 healthy US women, aged 45 years or older, from the
Women’s Health Study. These women reported overall physical activity
at baseline (1992-1995) and then
36, 72, 96, 125, and 149 months
later. During this lengthy period,
579 women developed incident
stroke: 473 ischemic strokes, 102
hemorrhagic strokes, and 4 strokes
of unknown type. Although intense
physical activity was not associated
with stroke risk (P = .50 for trend),
walking time and pace were inversely related to total, ischemic, and
hemorrhagic stroke risks (P = .002
through P = .07). Thus, all women
should be encouraged to try walking as a way to prevent stroke (and
other illnesses).
In a recent study, the effect of melatonin on breast and endometrial
cancers in women was examined.
Based on decades of scientific evidence, melatonin (N-acetyl-5-methoxytryptamine) is a hormone that
might protect against cancer development. Melatonin has antioxidant,
antimitotic, and antiangiogenic
properties. In addition, melatonin
alters fat metabolism and may regulate tumor growth. In terms of breast
cancer, melatonin may block an estrogen receptor (ie, ERα) and affect
aromatase (ie, an enzyme that produces estradiol). Epidemiologic
studies have examined the interaction between night shift work and
varied sleep duration and melatonin
concentration at night. The evidence indicates lower melatonin
concentration in those who work
the night shift. Case-control and
prospective cohort studies have indicated that the risk of breast and
endometrial cancers is affected by
night shift work. Overall, night shift
work may become a public health
concern if additional data indicate
its negative effect on cancer. More
studies should determine the exact
advantageous effects of melatonin
for the prevention of cancer.
Thyreoidea compositum, an antihomotoxic agent, may treat chronic
lymphocytic thyroiditis (autoimmune thyroiditis) in women who experience habitual miscarriage. In
this study, the therapeutic effectiveness of Thyreoidea compositum was
estimated in 28 women of reproductive age who had autoimmune thyroiditis and experienced habitual
loss of a fetus. The mean±SD age of
the women was 27.14±0.69 years,
and the mean±SD duration of the
disease was 1.57±0.16 years. Patients were divided into 3 groups:
(1) 9 women for whom L-thyroxin
was prescribed (control group); (2) 9
women who took Thyreoidea compositum, 2.2 mL, intramuscularly
once in 3 days (monotherapy); and
(3) 10 women for whom L-thyroxin,
50 to 100 μg/d, plus Thyreoidea
compositum (combination therapy)
was prescribed. The researchers determined that Thyreoidea compositum, used as both a monotherapy
and as part of a complex treatment,
leads to decreased levels of antibodies to thyroglobulin and thyrotropin,
an increased level of free thyroxine,
and goiter reduction. Therefore, this
antihomotoxic agent has immunecorrecting, anti-inflammatory, and
regenerative effects.
Stroke. 2010;41(6):1243-1250.
Cancer Lett. 2009;281(1):1-7.
doi:10.1016/j.canlet.2008.11.002.
Azerbaijan Med J. 2010;2:25-29.
Symptoms of peanut allergy usually
© iStockphoto.com/Don Bayley
© iStockphoto.com/Karen Sarraga
) What Else Is New?
appear rapidly and tend to be severe.
Exposure to urban air pollution may
increase breast cancer risk.
Infant Sensitivity to Peanut
Associated with Maternal
Ingestion
Endometriosis and
Leiomyomata Linked to
Phthalate Exposure
Air Pollution Affects
Breast Cancer Risk
Peanut allergies can be lifelong and
severe. In a recent study of 503 infants (age range, 3-15 months; mean
age, 9.4 months), maternal ingestion
of peanuts during pregnancy and
lactation affected the sensitivity of
infants to peanuts. The risk to the
infant increased with increased peanut intake by the mother. The infants studied had already experienced allergic reactions to other
products: 308 had an immediate reaction to cow’s milk and/or egg,
and 204 had atopic dermatitis and a
positive allergy test result to milk
and/or egg. Other significant factors that affected infant peanut allergy included male sex (P = .02)
and nonwhite race (P = .02).
Phthalates, chemicals in commercial
products, include mono(2-ethylhexyl) phthalate (MEHP), monobutyl
phthalate (MBP), monoethyl phthalate (MEP), and monobenzyl phthalate (MBzP). In this cross-sectional
study, mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) and
mono(2-ethyl-5-oxohexyl) phthalate were also examined. When a
population of women (aged 20-54
years) was studied to determine urinary phthalate levels, 7% and 12%
reported endometriosis and leiomyomata, respectively. The odds ratios
for MBP were as follows: 1.36 for
endometriosis, 1.56 for leiomyomata, and 1.71 for both conditions
combined.
J Allergy Clin Immunol.
2010;126(6):1191-1197.
Environ Health Perspect.
2010;118(6):825-832.
doi:10.1289/ehp.0901543.
An association was found between
the risk of breast cancer in postmenopausal women and exposure to
urban air pollution by measuring
concentrations of nitrogen dioxide
(NO2). The results of this case-control study conducted in Montreal,
Quebec, Canada, indicated that an
increase of 5-parts-per-billion NO2
produced an approximately 25% increased risk of breast cancer. The
NO2 is most likely part of a complex
mixture derived from combustion
and is not necessarily the causal factor but a marker of level of air pollution. Additional research is needed
to determine the possible critical periods of exposure to air pollution in
relation to breast cancer development.
Environ Health Perspect.
2010. doi:10.1289/ehp.1002221.
F O R P RO F E S S I ONA L U S E ON LY
The information contained in this journal is meant for professional use only, is meant to convey general and/or specific worldwide scientific information relating to the
products or ingredients referred to for informational purposes only, is not intended to be a recommendation with respect to the use of or benefits derived from the
products and/or ingredients (which may be different depending on the regulatory environment in your country), and is not intended to diagnose any illness, nor is it
intended to replace competent medical advice and practice. IAH or anyone connected to, or participating in this publication does not accept nor will it be liable
for any medical or legal responsibility for the reliance upon or the misinterpretation or misuse of the scientific, informational and educational content of the
articles in this journal.
The purpose of the Journal of Biomedical Therapy is to share worldwide scientific information about successful protocols from orthodox and complementary practitioners. The intent of the scientific information contained in this journal is not to “dispense recipes” but to provide practitioners with “practice information” for a better
understanding of the possibilities and limits of complementary and integrative therapies.
Some of the products referred to in articles may not be available in all countries in which the journal is made available, with the formulation described in any article or
available for sale with the conditions of use and/or claims indicated in the articles. It is the practitioner’s responsibility to use this information as applicable
and in a manner that is permitted in his or her respective jurisdiction based on the applicable regulatory environment. We encourage our readers to share
their complementary therapies, as the purpose of the Journal of Biomedical Therapy is to join together like-minded practitioners from around the globe.
Written permission is required to reproduce any of the enclosed material. The articles contained herein are not independently verified for accuracy or truth. They have
been provided to the Journal of Biomedical Therapy by the author and represent the thoughts, views and opinions of the article’s author.
) 13
) From the Practice
Uterine Fibroids
A Clinical Case Report
By Olga García Domínguez, MD
Gynecologist
F
) 14
ibroids or leiomyomas are the
most common form of benign
uterine tumor in women.1 Although
fibroids are found relatively rarely in
women younger than 20 years, statistically, 1 in 5 women of childbearing age will have this disorder.2
From the standpoint of conventional
medicine, the formation of fibroids
is considered a hormonal disturbance or the result of a genetic predisposition. Studies have also shown
that fibroids have different distributions among the various races.3 Fibroids are the result of increased
growth of smooth muscle tissue
within the uterus and its outer mucosa. The frequency distribution of
fibroid sites is as follows: subserous,
55%; intramural, 40%; and submucous, 5%.2
The symptoms of fibroids include
unusually heavy bleeding during
and between periods and nonspecific pressure in the lower abdomen,
associated with a frequent urge to
urinate and general bowel movement difficulties.4 In contrast, routine examinations sometimes reveal
fibroids that cause no symptoms.
The possibility that a fibroid will
follow a degenerative course is relatively rare. If fibroids become so
large that their blood supply is no
longer adequate, they may become
necrotic. In subserous fibroids, necrosis may also occur when fibroids
become twisted in on themselves
because of their abnormal size.2
Conventional medicine suggests
various treatment possibilities and
methods for use in fibroid therapy
that, as a rule, carry the risk of adverse effects. Surgical or drug treatment methods are used. The most
commonly used surgical procedures
are myomectomy, hysterectomy, and
drug-induced embolization via the
uterine artery. Pharmaceutical hormone treatments are also used (eg,
administration of a gonadotropinreleasing hormone analogue) to
trigger early menopause in the patient. The placement of intrauterine
devices that release hormones is another treatment method.5
From the standpoint of homotoxicology, fibroids are a chronic disease
that is classified in the deposition
phase and belongs to the germinodermal layer. It is assumed that the
disease is caused by multiple factors
and that psychological factors play a
particular role in this gynecological
disease. As an expert with long-term
experience in biological medicine, I
try, in my daily practice, to treat fibroid diseases primarily from a correspondingly different viewpoint.
Of course, every physician knows
that health is to be understood as an
unstable equilibrium state that is
constantly striving to balance itself
and that the neuroendocrine system
is involved in both human emotions
and the hormone cascade. Physicians can come closer to treating fibroid disease by carefully observing
the patient and getting to know
about her life history. This begins
with birth and includes dietary habits, emotional life, and physical activities. All of these individual characteristics are to be compiled in a
thorough history so that physicians
can successfully identify the factor
that caused the disturbance and led
to the disease.
I attempt to convey to the patient
that a fibroid constitutes an organic
enlargement in which nutrition
plays a role; therefore, I recommend
a diet according to the principles of
Traditional Chinese Medicine. I
combat the physical imbalance by
using homeopathically prepared
hormones and therapy with organ
extracts, which normalize the functions of the pituitary and thyroid.
Clinical Case
In 2009, a 43-year-old patient presented to my practice with massive
menstrual bleeding caused by an intramural fibroid measuring 8.1 x 6.6
cm (Figure 1). Her medical history
showed the following: menarche at
the age of 12 years, nullipara, 1 miscarriage, and no major diseases. Her
first fibroid symptoms had appeared
in 1994 at the age of 28 years. A
myomectomy was performed. In
January 2003, the fibroid symptoms
recurred. To counteract the renewed
heavy bleeding, which was having a
serious effect on her daily life, the
patient was treated with a hormonal
) From the Practice
Figure 1. Transabdominal Echography (2009)
Figure 2. Transvaginal Echography (2010)
subserous intramural fibroid on the anterior surface and right
The bilobular fibroid on the anterior surface is reduced,
An anteverted uterus, measuring 11.7 x 7.8 cm, is shown. A
border is clearly submucosal, measuring 8.1 x 6.6 cm.
intrauterine system. However, her
heavy bleeding continued, and the
fibroid continued to grow. According to the ultrasonographic examination results from 2007, the fibroid
had reached a size of 5.5 x 4.6 cm.
The severe bleeding persisted, and
the ultrasonographic examination
from 2008 showed that the fibroid
had grown to 7.0 x 5.4 cm. I immediately began homotoxicological
treatment and recommended the dietary adjustment, as discussed before.
Therapy
The patient received CinnamomumHomaccord in drop form (maximum
dosage, 70 drops daily) to counteract the heavy bleeding. For tissue
support, I administered Mucosa
com
positum ampoules (1 twice a
week). To reduce inflammation, she
was given Traumeel drops (10 drops
3-5 times a day). To slow the fibroid
growth and counteract obsessive
thoughts, I prescribed Thuja granules (5 granules daily); and for hormonal balance, I prescribed Agnus
An anteflected, large, and globular uterus.
measuring 6.6 x 4.5 cm.
castus granules (5 granules daily).
The latter medication is used to restore the balance between estrogens
and progesterone.
In the follow-up examination conducted by a colleague in February
2010, 6 months after the beginning
of treatment, the fibroid had decreased to 6.6 x 4.5 cm (Figure 2).
To date, the patient has remained
symptom free, and her menstrual
bleeding has become completely
normal. She continues to be treated
with the same medication. We await
the results of future regular ultrasonographic examinations of the
shrunken fibroid.|
References
1.Stewart EA. Uterine fibroids. Lancet.
2001;357(9252):293-298.
2. Katz VL. Benign gynecologic lesions: vulva,
vagina, cervix, uterus, oviduct, ovary. In:
Katz VL, Lentz GM, Lobo RA, Gershenson
DM, eds. Comprehensive Gynecology. 5th ed.
Philadelphia, PA: Mosby Elsevier; 2007:chap
18.
3. Blake RE. Leiomyomata uteri: hormonal and
molecular determinants of growth. J Natl
Med Assoc. 2007;99(10):1170-1184.
4. Levy BS. Modern management of uterine fibroids. Acta Obstet Gynecol Scand.
2008;87(8):812-823.
5. Viswanathan M, Hartmann K, McKoy N, et
al. Management of uterine fibroids: an update
of the evidence. Evid Rep Technol Assess (Full
Rep). 2007;(154):1-122.
Further reading
1. Cónill Montobbio V. Tratado de Gine
cología y de Técnica Terapéutica Gine
cológica. 5th ed. Barcelona, Spain: Labor; 1967.
2. Kushi M. Alimentacion Macrobiotica.
Madrid, Spain: EDAF; 2004.
3. Kyank H, Sommer K. Lehrbuch der
Gynäkologie. 3rd ed. Leipzig, Germany: Thieme; 1978.
4. Ordinatio Antihomotoxica et Materia
Medica: Tratado Práctico de Terapia
Antihomotóxica. 9th Rev ed. BadenBaden, Germany: Biologische Heilmittel Heel GmbH; 2007.
5. Pommier L. Diccionario Homeopático
de Urgencia. 2nd ed. Barcelona, Spain:
Paidotribo; 2002.
6. Schmid F, Rimpler M, Wemmer U.
Medicina Antihomotóxica: Principios,
Clínica, Práctica. Vol 1. 2nd ed. BadenBaden, Germany: Aurelia; 2004.
7. Vannier L. La Típologia y sus Aplicacio
nes Terapéuticas. Madrid, Spain: Mandala; 2001.
) 15
) Re f r e s h Yo u r H o m o t ox i c o l o g y
Which Came First:
Insulin Resistance or Inflammation?
) 16
By David W. Lescheid, PhD, ND
I
Although there are some similarities, the inflammatory component of
chronic diseases is different from the
inflammatory response associated
with tissue repair and recovery that
follows acute injury or infection.
This subclass of inflammation may
be termed metainflammation (metabolic inflammation), because of its
initiation by nutrients and metabolic
surplus5; or parainflammation, because it shares intermediate characteristics between the basal and acute
inflammatory state.6
Chronic inflammation does play an
important role in disease processes.
An important question to ask is as
follows: Why has the inflammation
occurred in the first place (ie, what is
the nature of the inflammatory inducer or trigger)? There are several
different theories and proposed
mechanisms; however, one of the
most promising current models suggests that dysregulated cell metabolism, particularly from nutrient excess and the associated altered
insulin signaling,7 is one of the most
important initiating events. This article will discuss the roles of hyperinsulinemia and of a few potential
triggers of excess insulin in the development of disease, with some examples of the effect on women’s
health issues.
Men and women have substantial
differences in body composition,
such as distribution of visceral and
hepatic adipose tissue and lean body
t is well established that persistently elevated levels of inflammatory cytokines play a significant role
in the development of chronic disease. For example, persistently high
levels of 1 or more of the proinflammatory cytokines (ie, interleukins 1
and 6 and tumor necrosis factor α)
are common to the pathogenesis of
diseases such as cardiovascular disease, cancers, inflammatory bowel
disease, chronic fatigue syndrome,
and neurological disorders (eg, depression, Parkinson disease, and
Alzheimer disease).1
The elevation of these cytokines has
become such a common thread for
the development of these diseases
that the term sickness behavior2,3 has
recently been proposed to describe
the associated signs and symptoms
of fever, anorexia, fatigue, sleepiness, and social withdrawal. Additional support for the paramount
importance of inflammation in disease development has recently come
from the Justification for the Use of
Statins in Primary Prevention: An
Intervention Trial Evaluating Rosuvastatin (JUPITER). The results of
this trial suggest that the proposed
benefit of statin drugs in the prevention of cardiovascular disease was
more likely because of their ability
to reduce levels of high-sensitivity
C-reactive protein (a nonspecific inflammatory marker) than their effects on lowering cholesterol.4
mass, and in sex hormone and adipokine levels. These differences tend
to improve insulin sensitivity in
women compared with men8 and
suggest that sex differences must be
considered when preventing and
treating diseases associated with insulin resistance.
There is no question that obesity has
reached epidemic proportions in
many parts of the world. In many
countries, particularly those of industrialized and developed nations,
there is a regular excess intake of
calories from increasingly caloriedense but nutrient-poor foods and
drinks. The excess of calories, combined with an increasingly less
physically active society, creates a
daily energy surplus that eventually
leads to a dysregulation of the
body’s key storage hormone, insulin
(Figure).9 With cells no longer sensitive to insulin and a surplus of blood
glucose triggering the continued release of insulin from the pancreas,
hyperinsulinemia develops.
Adipose tissue is an endocrine organ
releasing many different signaling
molecules, some of which have direct localized and systemic inflammatory effects.10 The development
of adipose tissue is preceded by an
impairment of energy balance that is
primarily associated with the inability of the cells to respond to insulin,
either through inadequacy of insulin receptor signaling or some other
defect in the biochemical pathway.
© iStockphoto.com/Martin McCarthy
Figure. Human
Insulin Molecule
Hyperinsulinemia
and Female Health
High insulin levels can modulate the
activity of gonadotropin-releasing
hormone in the hypothalamus (at
least in lean healthy controls) and,
therefore, interfere with the pattern
of release of luteinizing hormone
(LH).11 These data suggest that reproductive cycles, ovulation, and
fertility could be affected. Indeed,
recent evidence suggests that fasting
insulin levels, fasting serum levels of
sex hormone–binding globulin
(SHBG), and the free androgen index had strong negative influences
on the regularity of menstrual cycles
in young women.12 Furthermore,
women with insulin resistance and
hyperinsulinemia (and upper body
obesity, which is also termed android
or truncal obesity) had a greater risk
of anovulatory cycles13 that could be
reversed through the use of insulinsensitizing drugs.14
Glucose intolerance, including insulin resistance and impaired fasting
glucose level,15 is an important part
of the pathophysiological characteristics of polycystic ovary syndrome
(PCOS).16,17 However, insulin infusions to women with PCOS had no
effect on the secretion of LH, suggesting that the inappropriate secretion of LH observed in this disease
might not be directly due to insulin
resistance and hyperinsulinemia.18
Furthermore, there was no change
in the altered pattern of LH secretion in women with PCOS after insulin infusion despite an improvement in insulin sensitivity after
treatment with pioglitazone, a thiazolidinedione type of drug known
to modulate transcription of insulinsensitive genes in the muscle, liver,
and adipose tissue.19 This suggests
that the dysregulated gonadotropin
release in PCOS is caused by a
mechanism that is not directly related to insulin levels.
High insulin levels in the ovaries
help stimulate the production of steroid hormones, such as androstenedione and testosterone,20 that are
associated with some of the signs
and symptoms of disease in women
if they are in excess for a long time.
Higher levels of testosterone, but
not androstenedione, are correlated
with higher levels of insulin resistance in women (but not in men). In
particular, women with PCOS that
are also insulin resistant have the
highest circulating levels of testosterone, suggesting that their ovaries
are more sensitive to the testosterone-stimulating effects of insulin.21
Insulin is a key regulator of the synthesis of SHBG in the liver.22 Elevated levels of insulin down regulate
the production of SHBG and, therefore, increase the amount of bioavailable estrogen; this increases the
risk of diseases associated with estrogen excess. Furthermore, a decreased serum level of SHBG would
result in an excess of free testosterone and, therefore, the associated
signs and symptoms, such as hirsutism and acne. High testosterone and
low SHBG levels are also associated
with a higher risk of cardiovascular
disease in postmenopausal women.23
Elevated levels of insulin increase
the bioavailability of insulinlike
growth factor 1, by directly increasing its synthesis and decreasing several of its binding proteins (eg, insulinlike growth factor-binding proteins 1 and 2).24 Insulinlike growth
factor 1 is a hormone that is involved in several different conditions, including certain types of carcinogenesis,25 cognitive decline,26
dysregulation of the immune system, and autoimmune diseases,27
and in the development of female
disorders, including breast cancer in
premenopausal women.28
High insulin, but not insulinlike
growth factor 1, levels are independent risk factors for the development of breast cancer in postmenopausal women29 and for endometrial
adenocarcinoma.30,31
Possible Triggers of
Dysregulated Insulin Levels
The interconnectivity between female pathophysiological features
and insulin has been further substantiated with recent reports demonstrating that estrogen is important
in glucose homeostasis. For exam-
) 17
) 18
ple, both isoforms of estrogen receptor (α and β) are present in pancreatic beta cells. The insulin content
of pancreatic beta cells was increased
after long-term exposure to physiological levels of 17β-estradiol, most
likely by binding with estrogen receptor α.32
It is becoming increasingly evident
that environmental chemicals from
plastics and common household
products, such as bisphenol A (BPA)
and phthalates, have the potential to
trigger dysregulated metabolic
events that could lead to insulin resistance and contribute to the obesity epidemic.33 For example, there
is evidence that the environmental
estrogen mimetic BPA significantly
binds and activates estrogen receptor α in pancreatic beta cells at serum levels that are plausible, suggesting that this could be one of the
early triggers of dysregulated insulin levels. The putative role of BPA
in disrupting the normal physiological regulation of glucose has been
reported and reviewed elsewhere.34,35 It is interesting to note
that in mouse models, when pregnant mice are exposed to environmentally relevant levels of BPA, glucose homeostasis is affected and
insulin resistance develops not only
in the mothers themselves, but also
in the male offspring. These negative effects initiated in utero persisted until adulthood, suggesting that
exposure to BPA early in development could influence the development of chronic disease later in
life.36
Phthalates, widely found in plastic
products, are additional environmental pollutants that disrupt cellular metabolism and, therefore, contribute to the development of insulin
resistance and obesity (at least in
men).37 This dysregulation of cell
metabolism was the result of the
ability of phthalates to interfere
with the function of peroxisome
proliferative receptors,38 transcription factors known to function at a
critical intercellular junction between lipid and glucose metabolism
and, therefore, storage or usage of
nutrients.
A cellular event that might even precede insulin resistance and inflammation is endoplasmic reticulum
(ER) stress. This organelle can be
negatively affected by hypoxia, viral
infections, toxins, energy, and nutrient fluctuations (both deprivation
and excess of nutrients will stress
the ER), imbalances of calcium levels within the organelle, excess demands on host cell synthetic biochemical machinery, inflammatory
mediators, and accumulation of improperly processed proteins.11 The
ER responds to these stressors by a
complex response, known as the unfolded protein response, that ultimately initiates pathways that negatively affect insulin signaling and
promote the inflammatory response.5,7 The presence of chronic
oxidative stress, possibly from mitochondrial dysfunction, inadequate
cell antioxidant networks, or ER
stress, can promote insulin resistance
and inflammation and can impair insulin secretion from pancreatic beta
cells.5 Furthermore, persistent nutrient excess (and, ultimately, obesity)
increases the levels of excess free
fatty acids (that can activate inflammatory responses through binding
with toll-like receptors11), reduces
glucose availability (as the result of
cellular insulin resistance), and augments the demands for protein synthesis. These variables all induce ER
stress and the unfolded protein response.39 The ER might be the important sensory link between nutrient-associated signals and the
development of insulin resistance
and inflammation.11
It has recently been proposed that a
combination of nutrient excess and
physical inactivity, occurring against
a background of genetic predisposition, could lead to the persistent hyperglycemia associated with the development of oxidative stress.
Ultimately, this may trigger inflammatory pathways that contribute to
the development of chronic disease.
There are many different points
along this “oxidative inflammatory”
cascade that can be modulated to
prevent any pathological consequences; however, reducing the persistent hyperglycemia (by improving
insulin sensitivity) appears to be a
critical first step.40
In conditions of nutrient excess,
which are common in industrialized
nations, it is more likely that a dysregulation of metabolic signals, such
as insulin resistance, precedes the
promotion of the inflammatory response. These metabolic signals
could have been disrupted by stress
on intercellular organelles, such as
the ER, or, alternately, by external
stressors, such as the environmental
toxins BPA and phthalates. An increased understanding of some of
the key initiators of the process of
chronic disease can assist with the
development of prevention and
treatment plans that address the root
cause and, therefore, have a more
profound and persistent therapeutic
effect.|
References
1.Handschin C, Spiegelman BM. The
role of exercise and PGC1α in inflammation and chronic disease. Nature.
2008;454(7203):463-469.
2. Dantzer R, Kelley KW. Twenty years of research on cytokine-induced sickness behavior. Brain Behav Immun. 2007;21(2):153160.
3. Myers JS. Proinflammatory cytokines and
sickness behavior: implications for depression and cancer-related symptoms. Oncol
Nurs Forum. 2008;35(5):802-807.
4. Mora S, Ridker PM. Justification for the Use
of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER): can C-reactive protein be used to
target statin therapy in primary prevention?
Am J Cardiol. 2006;97(2A):33A-41A.
5. Hotamisligil GS, Erbay E. Nutrient sensing
and inflammation in metabolic diseases. Nat
Rev Immunol. 2008;8(12):923-934.
6. Medzhitov R. Inflammation 2010: new adventures of an old flame. Cell. 2010;140(6):
771-776.
7. Hotamisligil GS. Inflammation and metabolic
disorders. Nature. 2006;444(7121):860867.
8. Geer EB, Shen W. Gender differences in insulin resistance, body composition and energy
balance. Gend Med. 2009;6(suppl 1):60-75.
9. Fair AM, Montgomery K. Energy balance,
physical activity, and cancer risk. In: Verma
M, ed. Cancer Epidemiology. New York, NY:
Humana Press; 2009. Methods in Molecular
Biology; vol 472.
10. Wozniak SE, Gee LL, Wachtel MS, Frezza EE.
Adipose tissue: the new endocrine organ? A
review article. Dig Dis Sci. 2009;54(9):18471856.
11. Moret M, Stettler R, Rodieux F, et al. Insulin
modulation of luteinizing hormone secretion
in normal female volunteers and lean polycystic ovary syndrome patients. Neuroendocri
nology. 2009;89(2):131-139.
12. Wei S, Schmidt MD, Dwyer T, Norman RJ,
Venn AJ. Obesity and menstrual irregularity:
associations with SHBG, testosterone, and
insulin. Obesity. 2009;17(5):1070-1076.
13.Morán C, Hernández E, Ruíz JE, Fonseca
ME, Bermúdez JA, Zárate A. Upper body
obesity and hyperinsulinemia are associated with anovulation. Gynecol Obstet Invest.
1999;47(1):1-5.
14. Ibáñez L, Valls C, Ferrer A, Ong K, Dunger
DB, De Zegher F. Additive effects of insulin-sensitizing and anti-androgen treatment
in young, nonobese women with hyperinsulinism, hyperandrogenism, dyslipidemia,
and anovulation. J Clin Endocrinol Metab.
2002;87(6):2870-2874.
15. Salley KE, Wickham EP, Cheang KI, Essah
PA, Karjane NW, Nestler JE. Glucose intolerance in polycystic ovary syndrome: a position
statement of the Androgen Excess Society.
J Clin Endocrinol Metab. 2007;92(12):45464556.
16.Moran LJ, Misso ML, Wild RA, Norman
RJ. Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review
and meta-analysis. Hum Reprod Update.
2010;16(4):347-363.
17. Teede H, Deeks A, Moran L. Polycystic ovary
syndrome: a complex condition with psychological, reproductive and metabolic manifestations that impacts on health across the
lifespan. BMC Med. 2010;8:41.
18. Patel K, Coffler MS, Dahan MH, et al. Increased luteinizing hormone secretion in
women with polycystic ovary syndrome is
unaltered by prolonged insulin infusion.
19. Mehta RV, Patel KS, Coffler MS, et al. Luteinizing hormone secretion is not influenced
by insulin infusion in women with polycystic ovary syndrome despite improved insulin
sensitivity during pioglitazone treatment.
20. Franks S, Gilling-Smith C, Watson H, Willis
D. Insulin action in the normal and polycystic ovary. Endocrinol Metab Clin North Am.
1999;28(2):361-378.
21.Asagami T, Holmes TH, Reaven G. Differential effects of insulin sensitivity on androgens in obese women with polycystic ovary
syndrome or normal ovulation. Metabolism.
2008;57(10):1355-1360.
22.Franks S, Kiddy DS, Hamilton-Fairley D,
Bush A, Sharp PS, Reed MJ. The role of nutrition and insulin in the regulation of sex
hormone binding globulin. J Steroid Biochem
Mol Biol. 1991;39(5B):835-838.
23.Brand JS, van der Schouw YT. Testosterone, SHBG and cardiovascular health in
postmenopausal women. Int J Impot Res.
2010;22(2):91-104.
24. Kaaks R. Nutrition, insulin, IGF-1 metabolism and cancer risk: a summary of epidemiological evidence. Novartis Found Symp.
2004;262:247-260.
25.Renehan AG, Zwahlen M, Minder C,
O’Dwyer ST, Shalet SM, Egger M. Insulinlike growth factor (IGF)-I, IGF binding
protein-3, and cancer risk: systematic review and meta-regression analysis. Lancet.
2004;363(9418):1346-1353.
26. Sonntag WE, Ramsey M, Carter CS. Growth
hormone and insulin-like growth factor-1
(IGF-1) and their influence on cognitive aging. Ageing Res Rev. 2005;4(2):195-212.
27. Smith TJ. Insulin-like growth factor-I regulation of immune function: a potential therapeutic target in autoimmune diseases? Phar
macol Rev. 2010;62(2):199-236.
28. Key TJ, Appleby PN, Reeves GK, et al; Endogenous Hormones and Breast Cancer Collaborative Group. Insulin-like growth factor
1 (IGF1), IGF binding protein 3 (IGFBP3),
and breast cancer risk: pooled individual data
analysis of 17 prospective studies. Lancet On
col. 2010;11(6):530-542.
29.Gunter MJ, Hoover DR, Yu H, et al. Insulin, insulin-like growth factor-I, and risk of
breast cancer in postmenopausal women.
J Natl Cancer Inst. 2009;101(1):48-60.
30. Gunter MJ, Hoover DR, Yu H, et al. A prospective evaluation of insulin and insulin-like
growth factor-I as risk factors for endometrial cancer. Cancer Epidemiol Biomarkers
Prev. 2008;17(4):921-929.
31. Kaaks R, Lukanova A, Kurzer MS. Obesity,
endogenous hormones, and endometrial cancer risk: a synthetic review. Cancer Epidemiol
Biomark Prev. 2002;11(12):1531-1543.
32.Alonso-Magdalena P, Ropero AB, Carrera
MP, et al. Pancreatic insulin content regulation by the estrogen receptor ERα. PLoS One.
2008;3(4):e2069.
33.Desvergne B, Feige JN, Casals-Casas C.
PPAR-mediated activity of phthalates: a link
to the obesity epidemic? Mol Cell Endocrinol.
2009;304(1-2):43-48.
34. Alonso-Magdalena P, Morimoto S, Ripoll C,
Fuentes E, Nadal A. The estrogenic effect of
bisphenol A disrupts pancreatic β-cell function in vivo and induces insulin resistance.
Environ Health Perspect. 2006;114(1):106112.
35.Alonso-Magdalena P, Ropero AB, Soriano
S, Quesada I, Nadal A. Bisphenol-A: a new
diabetogenic factor? Hormones (Athens).
2010;9(2):118-126.
36. Alonso-Magdalena P, Vieira E, Soriano S, et
al. Bisphenol A exposure during pregnancy
disrupts glucose homeostasis in mothers and
adult male offspring. Environ Health Perspect.
2010;118(9):1243-1250
37. Stahlhut RW, van Wijngaarden E, Dye TD,
Cook S, Swan SH. Concentrations of urinary
phthalate metabolites are associated with
increased waist circumference and insulin
resistance in adult US males. Environ Health
Perspect. 2007;115(6):876-882.
38. Hurst CH, Waxman DJ. Activation of PPARα
and PPARγ by environmental phthalate
monoesters. Toxicol Sci. 2003;74(2):297308.
39.Gregor MF, Hotamisligil GS. Adipocyte
stress: the endoplasmic reticulum and metabolic disease. J Lipid Res. 2007;48(9):19051914.
40. Lamb RE, Goldstein BJ. Modulating an oxidative-inflammatory cascade: potential new
treatment strategy for improving glucose
metabolism, insulin resistance, and vascular
function. Int J Clin Pract. 2008;62(7):10871095.
) 19
) Practical Protocols
Genital Human
Papilloma Virus Infection
Bioregulatory Management
By Alta A. Smit, MD
The burden of human papilloma virus (HPV) infections
and their consequences is a major health concern worldwide in terms of the cost to society and suffering. It is
estimated that 360 million persons worldwide are infected
with HPV.1
O
) 20
f the 100 strains that exist,
only 40 have an affinity for
genital sites, being primarily sexually transmitted. These can be classified into 2 general categories: highand low-risk HPV. The low-risk
strains, especially types 6 and 11,
are responsible for genital warts and
respiratory papillomatosis. Of the
15 high-risk types, 2 strains (16 and
18) are responsible for approximately 70% of the cervical cancers
worldwide.2 Cervical cancer is the
second most frequent cancer of
women and is the first cancer caused
solely by virological agents.3
Human papilloma virus infection is
common, and most women will be
infected with 1 of the HPV subtypes
in their sexual lifetime. In most individuals, the infection is transient
and asymptomatic and will resolve
within 2 years.4 Only a subset of
women infected with high-risk carcinogenic HPV will develop invasive cervical cancer, and several cofactors have been associated with
HPV persistence and HPV-related
disease progression. These factors
include the following: (1) viral factors, such as genotype (eg, HPV
16)5; (2) lifestyle factors, such as tobacco smoke6 and long-term oral
contraceptive use7; and (3) genetic
and immunological host factors,
such as innate immunity.8
Prophylactic HPV vaccines have
proved to be highly effective in preventing HPV infection, despite concerns regarding their long-term
safety.9-11 However, even the rigorous vaccination program in industrialized countries will not obliterate
the need for cervical screening because the vaccine does not contain
all the carcinogenic viral types and
women already infected have no
benefit from the primary intervention.
Secondary prevention with cervical
screening has been extremely effective in reducing the serious sequelae
from HPV infection. In the future,
HPV screening (with or without cytological testing) may be used as the
primary screening test in women
older than 30 years.12
From a bioregulatory perspective,
the emphasis in treating HPV infection should be on the factors implicated in persistence and disease progression; the immunomodulatory
aspect and the tissue terrain should
be addressed in a primary fashion.
This type of treatment lends itself to
a classic 3-pillar approach (Table).
Lifestyle adjustment is of major importance, and smoking cessation
should especially be encouraged.
Protective sexual intercourse with
condoms is advised, especially in
women younger than 21 years because this is the age at which there is
a peak incidence and because the
presence of other sexually transmitted diseases concurrently has been
implicated in the persistence of
high-risk HPV types.|
References
1. Diaz ML. Human papilloma virus: prevention
and treatment. Obstet Gynecol Clin North Am.
2008;35(2):199-217, vii-viii.
2. Wheeler CM. Natural history of human papillomavirus infections, cytologic and histologic abnormalities, and cancer. Obstet Gyne
col Clin North Am. 2008;35(4):519-536, vii.
3. Garland SM, Hernandez-Avila M, Wheeler
CM, et al. Quadrivalent vaccine against human papillomavirus to prevent anogenital
diseases. N Engl J Med. 2007;356(19):19281943.
4. Steben M, Duarte-Franco E. Human papillomavirus infection: epidemiology and pathophysiology. Gynecol Oncol. 2007;107(2)
(suppl 1):S2-S5.
) Practical Protocols
Table. Three-Pillar Approach for the Treatment of HPV Infection
DET-Phase
Basic and/or
Symptomatic
Mucodermal
Urogenital
• Gynäcoheel
(inflammation)
Regulation Therapya
D&D
• Advanced supportive detoxification and drainageb
(for 6 weeks) followed by
• Basic detoxification and drainage: Detox-Kitc
(for 6 weeks)
Impregnation
IM
• Engystol
• Tonsilla compositum
(if persistence is not cleared by
a regimen with Engystol only)
COS
• Mucosa compositum
(vaginal and cervical)
• Cutis compositum
(external genital warts)
• Coenzyme compositum
• Ubichinon compositum
(if not cleared by the initial regimen)
Note: Persistent HPV is classified as being in the impregnation phase and, therefore, should be addressed aggressively. Engystol has been
shown to have antiviral properties in several viruses, including the DNA viruses,13 and can increase interferon production.14 Thus, it is used
as a supportive measure. However, if the virus is still persistent at the first follow-up after initiating treatment, a course of Tonsilla compositum (supportive of the immune system) and Ubichinon compositum (for deep cellular detoxification) should be added (3 times a
week for 6 weeks) and Engystol should be continued after this period with follow-up.
In patients who are seen with persistence of the same strain for longer than 2 years, these 2 organ regulators should be the first intervention for the first cycle, followed by Engystol.
Dosages: Gynäcoheel, 10 drops 3 times daily. Regulation therapy: tablets, 1 tablet 3 times daily; ampoules, 1 ampoule of each medication,
1 to 3 times per week; Detox-Kit, 30 drops of each medication in 1.5 L of water (drink throughout the day).
Abbreviations: COS, cell and organ support; D&D, detoxification and drainage; DET, Disease Evolution Table; HPV, human papilloma virus; IM,
immunomodulation.
a
Antihomotoxic regulation therapy consists of a 3-pillar approach: D&D, IM, and COS.
b
Advanced supportive detoxification and drainage consists of Hepar compositum (liver), Solidago compositum (kidney), and Thyreoidea
compositum (connective tissue).
c
The Detox-Kit consists of Lymphomyosot, Nux vomica-Homaccord, and Berberis-Homaccord.
5. Schiffman M, Herrero R, Desalle R, et al.
The carcinogenicity of human papillomavirus types reflects viral evolution. Virology.
2005;337(1):76-84.
6. McIntyre-Seltman K, Castle PE, Guido R,
Schiffman M, Wheeler CM. Smoking is a risk
factor for cervical intraepithelial neoplasia
grade 3 among oncogenic human papillomavirus DNA-positive women with equivocal or
mildly abnormal cytology. Cancer Epidemiol
Biomarkers Prev. 2005;14(5):1165-1170.
7. Marks M, Gravitt PE, Gupta SB, et al. The
association of hormonal contraceptive use
and HPV prevalence [published online ahead
of print October 26, 2010]. Int J Cancer.
doi:10.1002/ijc.25628.
8. Einstein MH, Schiller JT, Viscidi RP, et al.
Clinician’s guide to human papillomavirus
immunology: knowns and unknowns. Lancet
Infect Dis. 2009;9(6):347-356.
9. Haug C. The risks and benefits of HPV vaccination. JAMA. 2009;302(7):795-796.
10. Slade BA, Leidel L, Vellozzi C, et al. Postlicensure safety surveillance for quadrivalent
human papillomavirus recombinant vaccine.
JAMA. 2009;302(7):750-757.
11. Gold MS, McIntyre P. Human papillomavirus vaccine safety in Australia: experience to
date and issues for surveillance. Sex Health.
2010;7(3):320-324.
12. Waxman AG, Zsemlye MM. Preventing cervical cancer: the Pap test and the HPV vaccine. Med Clin North Am. 2008;92(5):10591082, x.
13. Oberbaum M, Glatthaar-Saalmüller B, Stolt
P, Weiser M. Antiviral activity of Engystol:
an in vitro analysis. J Altern Complement Med.
2005;11(5):855-862.
14.Roeska K, Seilheimer B. Antiviral activity of Engystol and Gripp-Heel: an in-vitro
assessment. J Immune Based Ther Vaccines.
2010;8:6. doi:10.1186/1476-8518-8-6.
) 21
) Specialized Applications
Contributions of
Biological Medicine in Infertility
By Gaston Orellana Alvarellos, MD
Infertility, defined as the inability to complete a pregnancy
within a reasonable period (usually 12 months) in cases in
which no contraceptives are used, is a problem that affects
1 in every 6 couples.1
A
lthough it is debatable whether
this figure has increased, it appears reasonably certain that women
have been increasingly postponing
their first pregnancy because of
their studies, work, or, simply, personal fulfillment. As we will see in
the following text, this produces a
complex situation that is of great
significance for biological medicine.2 Broadly speaking, the causes
of infertility can be summarized as
shown in the Figure.
Study centers specializing in infertility have developed well-designed
diagnostic methods, treatment protocols, and follow-up criteria that
are generally free of controversy.
Nevertheless, from the standpoint of
homotoxicology, which presupposes
a more holistic consideration of
each pathological event,4 I believe a
different light can be cast on this
particular subject. First, attention
must be focused on the 10% of cases
in which infertility is of unexplained
etiology, while remaining cognizant
of the fact that these considerations
are valid for all cases. In addition,
there is another area that has unex-
pectedly come to the forefront in
my personal experience; therefore, it
will be necessary to discuss this area
from a personal standpoint.
In Chile, a forum has been set up for
women being treated for infertility
to share their experiences on the Internet.5 In this forum, members have
mentioned the recurrent appearance
of studies promoting treatment referred to as “alternative” concurrently with conventional treatment. Because my name has appeared in
connection with successful cases, I
have had to assume responsibility
and consider, from both theoretical
and practical standpoints (in combination with acupuncture), the concepts I would like to share.
Most, if not all, of my patients have
been aged between 30 and 40 years.
This is what I mean when I say that
women have postponed pregnancy
until they have reached the age of
10%
10%
30%
Uterotubal factors
Male factors
20%
3
Figure. Causes of Infertility
Ovulatory factors
30%
Sperm mobility factors
Unexplained factors
) 22
approximately 35 years, a critical
point statistically with respect to
fertility.6
These are urban women, with sedentary jobs, working under artificial
light, eating the diet imposed by the
cafeteria at their company, in an environment that is overpopulated and
exposed to all of the toxins in a
modern building. The stress of modern life must be added, resulting
from a job in which one’s survival
depends on performance; this is
only one of the factors that contribute toward maintaining the body’s
alarm system on continual alert.
Relevant Biomedical Factors
1. Natural light. Circadian rhythms
and the role of melatonin must
be addressed. Melatonin is a hormone that was formerly paid little attention but whose study is
attracting ever-increasing interest, particularly with respect to a
scenario that is essentially cyclic.7
2. Physical exercise. Surprisingly, I
have been faced with the need
to recommend exercise and to
occasionally restrict it. Highper
formance physical exercise
causes severe disruption of the
hypothalamic-pituitary axis.8
3. Use of medicines. In particular,
medicines acting on the central
nervous system, which common-
© Monart Design/Fotolia.de
ly cause hyperprolactinemia,
should be examined.
4. Use of recreational drugs.
5.Nutrition.
• The consumption of complex
car
abohydrates, which are rich
in fiber and have a low glycemic
index, should be recommended.9
There is increasing impor
tance
attributed to insulin in fertility.10,11
• The consumption of proteins of
vegetable origin and white meat
is important. There is no need to
expand herein, but it is clear that
excessive amounts of arachidonic acid must be avoided. This ingredient is found in red meat and
contributes to the synthesis of
“bad eicosanoids.”12
• For the same reasons, with a
view to recommend the “good
eicosanoids”,12 the use of extravirgin and cold-pressed vegetable oils should be emphasized.
• Incidentally, when I speak of
good and bad eicosanoids, I am
drawing attention, in an extremely general manner, to factors that play a role in persistent
inflammatory syndrome and impaired endothelial function.
Bioregulatory Treatment
From the beginning of therapy, patients require the first pillar of treatment,4 detoxification and drainage,
using Nux vomica-Homaccord, Berberis-Homaccord, and Lymphomyo
sot. However, in practice, I have had
to administer the 2 other pillars earlier than planned because of the urgent nature of the patient’s situation.
Homotoxicology involves acceptance of the concept that there is a
minimum persistent inflammatory
syndrome behind every pathological situation. In practice, this implies
the use of Traumeel from the outset.
) 23
Table. Medications Used in the Treatment of Infertility
DET-Phase
Basic and/or
Symptomatic
Impregnation or
degeneration
• Gynäcoheel
Regulation Therapya
Optional
D&D
• Basic detoxification and
drainage: Detox Kitb
• China-Homaccord
(if patient has a depressed mood)
IM
• Traumeel
COS
• Ovarium compositum
• Placenta compositum
• Aesculus compositum
• Hepar compositum
• Coenzyme compositum
• Ubichinon compositum
Dosages: Gynäcoheel, 10 drops 3 times daily. Regulation therapy: tablets, 1 tablet 3 times daily; ampoules, 1 ampoule of each medication, 1
to 3 times per week; Detox-Kit, 30 drops of each medication in 1.5 L of water (drink throughout the day). Optional therapy: ampoules, 1
ampoule 1 to 3 times per week; drops, 10 drops 3 times daily.
Abbreviations: COS, cell and organ support; D&D, detoxification and drainage; DET, Disease Evolution Table; IM, immunomodulation.
a
Antihomotoxic regulation therapy consists of a 3-pillar approach: D&D, IM, and COS.
The Detox-Kit consists of Lymphomyosot, Nux vomica-Homaccord, and Berberis-Homaccord.
b
) 24
Clinicians are faced with a problem
in which there is no clarity about
the specific organ that requires support. From a simplistic point of
view, the ovary must be considered
as the main organ responsible; however, infertility is a problem of unknown origin. From this perspective, what I propose and use, in
addition to Ovarium compositum, is
Hepar compositum because the metabolism of steroids requires a
healthy liver. If the dysfunctional
tissue is unknown, I propose Coenzyme compositum and Ubichinon
compositum as a second step.
There are 2 resources that also must
be mentioned. The first is Sepia in
potency chords, as is seen in ChinaHomaccord, which meets the needs
of a depressed and hopeless patient
who requires support.
The second is Placenta compositum.
I have the highest opinion of its ca-
pacity to increase microcirculation
at any level, including the ovaries; if
applicable, this capacity should be
considered.
The bioregulatory treatment of
infertility is summarized in the
Table.|
References
1. Lim AS, Tsakok MF. Age-related decline in
fertility: a link to degenerative oocytes? Fertil
Steril. 1997;68(2):265-271.
2. Cruz JR, Gindoff PR. Age and reproduction.
Reprod Med Rev. 1999;7(1):61-69.
3. Edwards RG, Risquez F, eds. Modern Assisted
Conception. Cambridge, England: Reproductive Healthcare Ltd; 2003.
4. Ordinatio Antihomotoxica et Materia Medica:
Tratado Práctico de Terapia Antihomotóxica.
6th Rev ed. Baden-Baden, Germany: Biologische Heilmittel Heel GmbH; 2002.
5. Foro Del Zócalo–Infertilidad–Adopción. Zócalo Web site. http://www.forodelzocalo.cl/.
Accessed May 2, 2011.
6. Age and Fertility: A Guide to Patients. American Society of Reproductive Medicine Web
site. http://www.asrm.org/uploadedFiles/
ASRM_Content/Resources/Patient_Resources/Fact_Sheets_and_Info_Booklets/
agefertility.pdf. Accessed May 2, 2011.
7. Lewy AJ. Melatonin and human chronobiology. Cold Spring Harb Symp Quant Biol.
2007;72:623-636.
8. Stafford DE. Altered hypothalamic-pituitary-ovarian axis function in young female
athletes: implications and recommendations for management. Treat Endocrinol.
2005;4(3):147-154.
9. Chavarro JE, Rich-Edwards JW, Rosner BA,
Willett WC. A prospective study of dietary
carbohydrate quantity and quality in relation
to risk of ovulatory infertility. Eur J Clin Nutr.
2009;63(1):78-86.
10.Kasturi SS, Tannir J, Brannigan RE. The
metabolic syndrome and male infertility.
J Androl. 2008;29(3):251-259.
11. Porte D Jr, Baskin DG, Schwartz MW. Insulin signaling in the central nervous system:
insulin and the control of reproduction and
lifespan in mammals. Medscape Today Web
site. http://www.medscape.com/viewarticle/504336_13. Accessed May 2, 2011.
12. Sears B. The Anti-aging Zone. New York, NY:
Regan Books; 1999.
) Meet the Expert
Dr. Mónica Lucia
Name Guerra
By Edda Medina, MD
B
orn in Sincelejo, Colombia,
Mónica grew up with her parents, Judith and Assad, and at the
side of her three brothers. Music,
poetry, and medicine were the constant components of her surroundings and predicted her successful
life. From a very early age, and
thanks to her father, a psychiatrist,
and her uncle, a plastic surgeon,
Mónica was in close contact with
medicine, the profession to which
she was to devote all her energy.
After graduating with a medical degree from the Universidad del Norte
in Barranquilla, and with the firm
intention of specializing in plastic
surgery, she found her life taking an
unexpected turn. She witnessed the
return to health of her father, who
had been treated with alternative
therapy by a friend from his university days, Armando Rojas, who had
dedicated himself to antihomotoxic
medicine. The biological physician
invited her to spend her vacation at
the Center for Biological Medicine
in Cali (founded by Dr. Arturo
O’Byrne), and Mónica
gladly accepted.
During this period,
her contact with the world of integrative biological medicine gave her
the opportunity to witness not only
the results achieved in patients, but
also the possibility of practicing
medicine in a holistic and integrative manner. What was planned as a
brief vacation turned into a 5-year
stay, beginning in 1991, during
which she was trained in biological
medicine and homotoxicology.
Mónica came to realize the diagnostic and therapeutic benefits of electroacupuncture under the supervision of Dr. O’Byrne. Her interest
and research led her to write a book
in 2000, entitled Electroacupuntura
de Voll (Electroacupuncture After
Voll), promoting the appropriate use
and interpretation of this diagnostic
and therapeutic method.
Thanks to the support of her husband, William Rincón, with whom
she has shared her life since 1999,
she began a successful medical career, resulting in the founding of her
clinic in Bogota, which serves as a
center of integrative biological medicine.
The young couple fulfilled their
lives with the birth of their son,
William David, who became Mónica’s central inspiration, driving her
to be more creative, dynamic, and
enterprising. She enrolled at the National University of Colombia in
2000, where she completed a variJournal of Biomedical Therapy 2011 ) Vol. 5, No. 1
ety of additional courses in cellular
and molecular biology, osteopathy,
neural therapy, and acupuncture.
She completed her studies and obtained a master’s degree in homeopathy in 2009.
Mónica’s interest in academia has
led her to develop accredited programs in molecular biology, with a
specialty in homotoxicology, at several nationally and internationally
recognized universities in various
cities in Colombia.
Mónica’s versatility and dedication
are also reflected in her choice of
pastime activities. She is an accomplished singer and has mastered
both the piano and the guitar. In addition, she enjoys painting and
practicing her most daring hobby:
riding the unicycle.|
) 25
) E x p a n d Yo u r Re s e a r c h K n o w l e d g e
Purpose-Orientated
Clinical Research
By Robbert van Haselen, MSc
In the previous article in this series, I provided an overview of the different medical study formats. Reference was
made to an “evidence mosaic” as a multifaceted evidence
base. In this article, I will delve a bit deeper into the role
of clinical research as part of the evidence base.
I
) 26
n terms of research design, clinical studies can be interventional
(clinical trials) or noninterventional
(various types of observational studies).
Clinical trials are experiments in
which patients are usually allocated
to groups at random (ie, randomized) and exposed to different treatments, with the goal of obtaining an
unbiased comparison. Clinical trials
can be either single blind (the nature
of treatment is “masked” only for
the patient) or double blind (the treatment is masked for both physicians
and patients). Sometimes, reference
is made to triple blind (usually this
means that all the principal statistical analyses are completed on a
blinded basis before the treatment
allocation code is broken). In cases
in which blinding of treatment is
not possible, the term open label is
often used.
There are many types of observational studies. The key design characteristic is that these studies are
noninterventional. The most basic
type of observational study is a case
report. Further types of observation-
al studies are case series, case-control studies, and cohort studies. Cohorts can be defined in different
ways (eg, on the basis of exposure to
toxic substances, such as tobacco
smoke, or treatment[s] received).
The latter studies are sometimes referred to as postmarketing surveillance
studies. Such cohort studies are useful for collecting information on the
safety and effectiveness of particular
medicines or therapeutic approaches
in routine clinical practice. In summary, the key feature that distinguishes observational studies from
clinical trials is the absence of an
experimental intervention.
A postauthorization safety study (PASS)
is defined as a pharmacoepidemiological study performed in accordance with the terms of the marketing authorization, conducted with
the aim of identifying or quantifying a safety hazard related to an
authorized medicinal product.1
Therefore, a PASS is primarily characterized by its objective and not by
its design. For instance, there is a
PASS using an interventional design
that confirms the safety of Traumeel
tablets.2 On the other hand, there
are numerous noninterventional
(PASS) cohort studies, including approximately 9000 patients, that
confirm the excellent tolerability of
Traumeel in its various galenic
forms.3 Therefore, PASSs are important for further substantiating the
excellent safety profile of biotherapeutic medicines. It is often forgotten that the utility of a treatment is
not only determined by its effectiveness but also by its safety, often referred to as the risk-benefit ratio.
Therefore, the relative safety of bioregulatory compared with conventional medicine is an important factor in conveying the overall utility
of the therapeutic approach.
The characteristics of the previously
mentioned study designs are summarized in the Table.
Dimensions of Research Design
The purposes of clinical research on
products can be categorized in various dimensions. The main types of
clinical studies are positioned somewhere in a space with the dimensions reality (real world vs ideal
world), comparativeness (absolute
effects vs relative effects), and level
of confirmation (hypothesis generation vs hypothesis confirmation).
Real World vs Ideal World
This dimension is illustrated by contrasting the determination of relative efficacy of a treatment vs place-
Table. Characteristics of Clinical Study Designs
Study Design
Characteristics
Randomized
This is an interventional study in which participants are randomly (ie, by chance) assigned to 1 of 2 or more
clinical trial
treatment arms. The reference treatment can be a placebo and/or an active treatment.
A pragmatic clinical trial aims to assess the effectiveness of a treatment as much as possible under “realworld” conditions (ie, “Does it work?”).
An explanatory clinical trial aims to assess the efficacy of a treatment under ideal conditions (ie, “Can it
work?”)
Postauthori
This is a pharmacoepidemiological study performed in accordance with the terms of the marketing authori-
study
medicinal product.
zation safety
Cohort study
zation, conducted with the aim of identifying or quantifying a safety hazard related to an authorized
This type of study involves the identification of 2 or more cohorts of patients, one receiving the exposure/
treatment of interest and the other(s) not, and following up these cohorts with regard to the outcome of
interest.
Case-control
study
This type of study involves the identification of patients who have the outcome of interest and control
patients who do not have the outcome of interest and then looking back to see if they had the exposure/
treatment of interest.
bo in the “ideal world” of highly
preselected patients who are willing
to participate in a clinical trial vs determining the effectiveness of a
treatment in patients in the “naturalistic” setting of routine clinical practice in observational studies. This
dimension is weighted differently
depending on the perspective. For
health economists, real-world costeffectiveness data are more valuable
than placebo-controlled clinical trial
data. On the other hand, for a competent authority (ie, government
regulatory body) that needs to decide on allowing a new drug on the
market for a particular indication,
placebo-controlled data will often
be preferred. Most clinicians will
usually want to know the effectiveness of a proposed new treatment
compared with existing treatments.
Absolute vs Relative Effects
As an example, a clinical case report
ranks the highest on the scale of
“absolute effectiveness”; on the other hand, a clinical trial comparing
the new treatment of interest with
the best available alternative treat-
ment ranks the highest on the scale
of “relative efficacy.”
Hypothesis Generation vs
Hypothesis Confirmation
Most observational studies are excellent hypothesis-generating tools.
In such cases, a “proof-of-concept”
clinical pilot trial could be a next
step in identifying the most promising hypotheses, which can then be
confirmed in larger-scale “confirmatory trials.”
The Figure illustrates how different
study designs fit into these dimensions. As can be seen from the positioning on the top-to-bottom axis,
clinical case reports represent maximally the “real world” of clinical
practice. When looking at the horizontal axes, it can be seen from the
positioning on the left-to-right axis
that case reports primarily represent
“absolute” rather than “relative” effects. The reason for this is obvious:
in a single case, clinicians are only
interested in the effect in that particular patient and not in comparing
it with effects in other patients.
From the positioning on the frontto-back axis, it is clear that clinical
case reports are primarily hypothesis generating. The reason for this is
that a single case report can rarely
be a definite proof. A case series,
pointing in the direction of a particular outcome, is still primarily hypothesis generating, but compared
with a single case report, similar observations in repeated cases can be a
first step toward confirmation of a
particular hypothesis. The latter is
represented by a shift in the direction of hypothesis confirmation on
the front-to-back axis.
All the clinical trial designs are on
the horizontal axes, firmly placed
toward hypothesis confirmation and
relative effects. The reason is related
to the primary objective of clinical
trials: to make comparisons between
different treatments to confirm or
refute a particular predefined hypothesis. The main variation occurs
on the vertical axis. A trial with a
“surrogate” marker (eg, a particular
laboratory value deemed to be predictive of a particular outcome) is
less representative of the real world
) 27
Ideal World
ts
ffec
te E
Hypothe
sis Confi
rmat
olu
Abs
Clinical Trial vs Placebo
Clinical Outcome
ion
Cohort
Studies
Case
Control
Studies
Hypoth
esis Ge
neratio
n
Pragmatic Clinical Trial
Active Control
Postauthorization
Safety Study:
Noninterventional
Case Series
s
ct
ffe
E
e
tiv
a
l
Re
© iStockphoto.com/Kheng Guan Toh
Postauthorization
Safety Study:
Interventional
Clinical Trial vs Placebo
Surrogate Marker
Real World
Clinical
Case Report
Figure. Positioning of Clinical Study Designs
on 3 Key Research Design Dimensions
) 28
than a placebo-controlled trial with
a clinical outcome measure (eg,
pain). Also, placebo-controlled trials
are less representative of the real
world compared with trials in which
the treatment of interest is compared
with a well-established active treatment.
In between case reports and clinical
trials, which are positioned toward
the extremes of the 3-dimensional
space in the Figure, there are several
further study types, such as casecontrol studies, cohort studies, and
PASSs.
Irrespective of whether a clinical
study is a clinical trial or a case report, from a scientific perspective,
the value of a study is determined by
the appropriateness of the chosen
design and the quality of its reporting.|
References
1. EudraLex - Volume 9 Pharmacovigilance
guidelines. European Commission Web site.
http://ec.europa.eu/health/documents/eudralex/vol-9/index_en.htm. Accessed May
2, 2011.
2. Arora S, Harris T, Scherer S. Clinical safety
of a homeopathic preparation. Biomed Ther.
2000;18(2):222-225.
3. Data on file. Baden-Baden, Germany: Biologische Heilmittel GmbH.
) Around the Globe
Fifth International Congress on
Complementary Medicine Research
Tromsø, Norway, May 18 to 21, 2010
By Konstantin Cesnulevicius, MD, PhD
T
pathic pathogenetic trials (provings).
He recommended developing methods for screening participants for
sensitivity to the medicine used and
establishing standards of planning,
conducting, reporting, and communicating provings.
Rainer Lüdtke presented the results
of a systematic review that compared placebo effects in clinical trials on homeopathy with placebo effects in trials using conventional
therapies. Results showed that, contrary to what is often assumed, placebo effects in randomized controlled trials using classical
homeopathy were no larger than
placebo effects using conventional
medicine. This means that all
schools of homeopathy can, in principle, be investigated in placebocontrolled studies. This study has
been published in Homeopathy.1
Many presentations focused on
“comparative effectiveness research”
and the methodological challenges
in CAM research. Issues that were
discussed intensively during the
congress included the “atypical” patient populations used in CAM research (compared with patients seen
in routine CAM practice), blinding
issues (eg, in acupuncture), the need
for sensitive and appropriate outcome measures, and highly “context-specific” results of clinical studies.
Josephine Briggs, MD, director of
the US National Center for Comple-
he International Congress on
Complementary Medicine Research in Tromsø, Norway, was an
intensive 4-day event involving 6
keynote, 160 oral, and 110 poster
presentations, as well as 5 symposia.
The International Congress on
Complementary Medicine Research
2010 was the fifth congress of the
International Society for Complementary Medicine Research; these
congresses take place on a yearly rotating basis in Europe, Australasia,
and the Americas. The fact that so
many complementary and alternative medicine (CAM) researchers
from throughout the world were
willing to travel such long distances
further underlined the rapid increase
of CAM research activity on a global scale. Dominant CAM treatment
modalities were Chinese medicine,
acupuncture, body-mind techniques,
and homeopathy.
Several basic research studies on homeopathy were presented, including
data from Kerstin Röska, PhD, suggesting that Engystol stimulates antiviral interferon type I production
in cells of the innate immune system
in vitro and that it might have a potent antiviral effect. Stephan
Baumgartner, PhD, presented studies that suggested there were biological effects of potentized substances, including rosy apple aphid
and Arsenicum album.
Jim Rogers gave an interesting presentation on the methods of homeo-
mentary and Alternative Medicine,
gave a keynote lecture on CAM research. She highlighted that there is
a need for “pharmacological signatures” of natural products to evaluate
them properly in clinical trials.
These pharmacological signatures
are important for demonstrating and
explaining changes in actual pathophysiological mechanisms.
The quality and professionalism of
CAM research are rapidly evolving
further; the fifth congress of the International Society for Complementary Medicine Research has illustrated and confirmed this trend.
Abstracts of the conference can be
downloaded from the International
Congress on Complementary Medicine Research 2010 web site.2
The congress also confirmed that
more basic and clinical research is
needed in homeopathy. The sixth
congress of the International Society for Complementary Medicine
Research will take place in Chengdu, China, from May 7 to 9,
2011.|
References
1. Nuhn T, Lüdtke R, Geraedts M. Placebo
effect sizes in homeopathic compared to
conventional drugs: a systematic review of
randomised controlled trials. Homeopathy.
2010;99(1):7682.
2. ICCMR 2010 Abstract Book. Rev ed. ICCMR 2010 Web site. http://www.iccmr2010.
com/Media/Files/ICCMR-2010-AbstractBook-Revised-Edition. Accessed May 2,
2010.
) 29
) Re s e a r c h H i g h l i g h t s
Traumeel for the Treatment of Pain
Associated With Breast Cancer
Summary
) 30
By Gaston Orellana Alvarellos, MD
Introduction
Breast cancer is a worldwide problem because of its high incidence.
The pain associated with breast cancer treatment, including surgery, radiotherapy, and chemotherapy, often
remains a long-term problem for
many patients. The pain can be a result of scars after surgery or the adverse effects of radiotherapy and
chemotherapy. This pain can definitely affect the quality of life of patients. Therefore, effective pain
treatments are important.
The World Health Organization
lists the following conventional
treatments for pain associated with
breast cancer: acetylsalicylic acid,
paracetamol, naproxen, metamizol,
and diclofenac (step 1 nonsteroidal
anti-inflammatory drugs); and tramadol, codeine, and dihydrocodeine
(step 2 opioid analgesic agents).
However, these conventional treatments may not be effective for all
patients who experience pain associated with breast cancer. Therefore,
the following complementary and
alternative therapies may also be
used (especially for short-term pain
relief ): acupuncture, hypnosis, relaxation/imagery, music, massage,
and herbal supplements. Finally, homotoxicological treatments, such as
Traumeel (Heel GmbH, BadenBaden, Germany), can be used to
treat resistant pain associated with
breast cancer.
In the study by Orellana Alvarellos
et al,1 a Traumeel injection was used
to alleviate the pain associated with
breast cancer for patients who continued to experience pain after treatment with conventional medications. This study showed the
advantages of Traumeel injection
therapy for the relief of pain in those
with breast cancer.
Methods
The study by Orellana Alvarellos et
al1 included case observations of 9
women with unilateral breast cancer.
The study was performed to assess
pain relief and health-related quality
of life after use of Traumeel injection therapy.
The 9 women in this study were
aged 52 to 81 years (mean, 69.7
years). The cancer treatment these
women received included surgery
(conservative in 6 women and radical in 3 women), radiotherapy (all 9
women), and chemotherapy (only 3
women). Some of the women experienced pain immediately after treatment, whereas others only experienced pain between 2 and 12
months after surgery plus radiotherapy. The conventional pain medications that the women received after
treatment included paracetamol,
pregabalin, ibuprofen, and ketoprofen. (One woman did not receive
any of these medications.).
A combination Traumeel and procaine injection was administered to
all 9 women, who were then observed from August 2007 to April
2008. The Traumeel injection soluJournal of Biomedical Therapy 2011 ) Vol. 5, No. 1
tion contained the following active
ingredients: Arnica montana, Calen
dula officinalis, Chamomilla recutita,
Symphytum officinale, Achillea mille
folium, Atropa belladonna, Aconitum
napellus, Bellis perennis, Hypericum
perforatum, Echinacea angustifolia,
Echinacea purpurea, Hamamelis virgin
iana, Mercurius solubilis Hahnemanni,
and Hepar sulfuris. The injection
was given once weekly (1 ampoule
[2.2 mL] of Traumeel given subcutaneously with 2% procaine [5.0 mL]).
Procaine was added to the Traumeel
injection to relieve the pain associated with the injection. There were
a maximum of 20 sites for injection
(based on Oriental acupuncture), including the breast, ipsilateral shoulder, and ipsilateral scapula.
The 9 women received from 3 to 10
injections, until the pain was reduced. Injections were administered
weekly. After the last injection, the
patients were observed for 3- and
6-month periods. Of the 9 patients,
7 completed 6 months of observation and 2 completed 3 months of
observation.
Pain was assessed by the 9 women
as follows: before injection, immediately after injection, and at the 3and 6-month observations. The
sites, type, and occurrence of pain
were assessed by questionnaire.
Pain level was determined on a scale
from 1 to 10, as on a visual analog
pain scale. Patients also rated their
health-related quality of life, including physical disability, insomnia,
Results
Three months after the final Traumeel injection, the mean±SD pain
score was 3.3±2.2 points (range,
1-7 points). This indicated a slight
overall increase in pain when compared with the level immediately
after the Traumeel injection. However, at 3 months after the final
treatment, the effects of Traumeel
injection therapy tended to vary
from patient to patient. For example,
1 patient experienced further pain
relief, from 4 to 2 points; 3 patients
maintained their pain relief (between 1 and 3 points); and 5 patients experienced increased levels
of pain (between 2 and 7 points).
Overall, all 9 women still had lower
levels of pain than they had before
the Traumeel injection was first administered.
Six months after the final Traumeel
injection, the mean±SD pain score
was 4.1±2.5 points (range, 1-7
points). For 5 of the women, the
pain score remained the same; only
2 women experienced increased
pain (this increase did not require
treatment). Overall, the pain score
was lower than before treatment,
even after a lengthy period without
any further therapy. Finally, even 12
months after the last Traumeel injection, some of the women noted that
their pain had not been exacerbated.
In terms of physical disability, insomnia, and psychological distress
symptoms, all 9 women experienced
improvement after Traumeel injection therapy. At the 3-month obser-
© iStockphoto.com/cunfek
© iStockphoto.com/motorolka
and psychological distress. Finally,
use of conventional analgesic agents
before and after the Traumeel injection was noted.
) Re s e a r c h H i g h l i g h t s
The active ingredients of Traumeel
include two species of the purple
coneflower (Echinacea angustifolia and
Echinacea purpurea, left) and the
common daisy (Bellis perennis, right).
vation, this improvement was sustained and even further increased in
most of the women. However, 2
women experienced a deterioration
in these quality-of-life variables (to
levels before the Traumeel injection). At the 6-month observation, 7
women continued to sustain a good
quality of life, as determined by the
physical and psychological symptoms.
The patients were asked about the
effectiveness of Traumeel injection
therapy. Of the 9 women, 8 indicated high effectiveness and 1 indicated good effectiveness. No patients reported low effectiveness.
Overall, Traumeel injection therapy
in these 9 women with breast cancer
produced a sustained reduction in
pain. Therapy also helped these
women improve their management
of daily work and reduce their psychological distress. Finally, the
women experienced improved sleep
as well.
Discussion
Traumeel has been used in Germany
since 1937 to treat injuries and trauma. Research has indicated that
Traumeel has analgesic and anti-inflammatory properties “by inhibiting the release of proinflammatory
cytokines” (ie, interleukin 1β and
tumor necrosis factor α) and a chemokine (ie, interleukin 8) in vitro.2
Other indications for which Traumeel has been used include chemotherapy-induced stomatitis, pain,
and inflammation.
The pilot study performed by Orellana Alvarellos et al1 determined the
effect of Traumeel injection therapy
on 9 women with breast cancer. It
was an open-label study and was
not blinded. Each of the 9 women
had taken various analgesic agents
before the injection therapy, and the
dosages of these agents were variable.
This study is the first to show the
effectiveness of Traumeel injection
therapy for pain associated with
breast cancer. For example, 1 of the
9 women reduced her pain level
from 10 points before the Traumeel
injection to 5 points at 6 months after the last injection. Traumeel is effective because it contains neuralgia-alleviating substances used in
homeopathy and homotoxicology.
In conclusion, Traumeel injection
therapy should be considered as an
alternative therapy for pain in patients with breast cancer. Because
breast cancer remains a worldwide
health issue, and patients continue
to experience resistant pain, effective pain medications are important.
Traumeel provided tremendous pain
relief immediately after final administration. This pain relief was long
lasting (without using additional
therapeutic agents). Therefore, because the results with Traumeel were
good in this study, further clinical
trials of this effective and tolerable
homotoxicological agent should be
planned and conducted.|
References
1. Orellana Alvarellos G, Ruiz de Viñaspre
Alvear P, Kaszkin-Bettag M. A series of
case reports: clinical evaluation of a complex homeopathic injection therapy in the
management of pain in patients after breast
cancer treatment. Altern Ther Health Med.
2010;16(1):54-59.
2. Porozov S, Cahalon L, Weiser M, Branski
D, Lider O, Oberbaum M. Inhibition of IL1beta and TNF-alpha secretion from resting
and activated human immunocytes by the
homeopathic medication Traumeel S. Clin
Dev Immunol. 2004;11(2):143-149.
) 31
IAH Abbreviated
Course
An e-learning course leading to
certification in homotoxicology
from the International Academy for
Homotoxicology in just 40 hours.
1 Access the IAH website at www.iah-online.com. Select your language.
2 Click on Login and register.
3 Go to Education Program.
4 Click on The IAH abbreviated course.
5 When you have finished the course, click on Examination.
After completing it successfully, you will receive your
certificate by mail.
For MDs and licensed healthcare practitioners only
Free of charge
) 32
www.iah-online.com

Biomedical Therapy - International Academy of Homotoxicology

Transcription

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